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Altered Nrf2-Keap1-ARE (Nuclear factor erythroid-2-related factor 2-Kelch-like ECH-associated protein 1-Antioxidant responsive element) and SIRT1 (Sirtuin 1) cell signaling pathways are considered to play major role in the etiology and pathogenesis of Alzheimer’s disease (AD) and Parkinson’s disease (PD). Strikingly, betanin, a betanidin 5-O-β-D-glucoside compound is reported to show commendable anti-oxidative, anti-inflammatory and anti-apoptotic effects in several disease studies including AD and PD. The present review discusses the pre-clinical studies demonstrating the neuroprotective effects of betanin by virtue of its potential to ameliorate oxidative stress, neuroinflammation, abnormal protein aggregation and cell death. It highlights the direct linkage between the neuroprotective abilities of betanin and upregulation of the Nrf2-Keap1-ARE and SIRT1 signaling pathways. The review further hypothesizes the involvement of the betanin-Nrf2-ARE route in the inhibition of beta-amyloid aggregation through beta-site amyloid precursor protein cleaving enzyme 1 (BACE1), one of the pivotal hallmarks of AD. The present review hereby for the first time elaborately discusses the reported neuroprotective abilities of betanin and decodes the Nrf2 and SIRT1 modulating potential of betanin as a primary mechanism of action behind, hence highlighting it as a novel drug candidate for the treatment of neurodegenerative diseases in the near future.",{"EN":111,"VI":112},"Traversing through the cell signaling pathways of neuroprotection by betanin: therapeutic relevance to Alzheimer’s Disease and Parkinson’s Disease","Khảo sát các con đường tín hiệu tế bào bảo vệ thần kinh của betanin: ý nghĩa điều trị đối với bệnh Alzheimer và bệnh Parkinson",{"VOID":114},"Abedimanesh N, Asghari S, Mohammadnejad K, Daneshvar Z, Rahmani S, Shokoohi S, Farzaneh AH, Hosseini SH, Jafari Anarkooli I, Noubarani M, Andalib S, Eskandari MR, Motlagh B (2021) The anti-diabetic effects of betanin in streptozotocin-induced diabetic rats through modulating AMPK\u002FSIRT1\u002FNF-κB signaling pathway. 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overview of computer-assisted diagnostic software",{"VOID":299},"[\"17630705565314546868\"]",{"VOID":301},"10.1007\u002FBF00999724","2024-04-28T02:13:01.903+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00999724",[305],{"id":306,"sortIndex":23,"researcher":22,"roles":307,"affiliations":308,"properties":317,"displayName":319,"givenName":22,"familyName":22},"9ae47ec7-1679-4099-a61d-244a6e28b466",[128],[309],{"id":310,"sortIndex":23,"affiliation":311,"properties":22},"30543460-0148-453f-9dcf-5486eeb08e35",{"id":310,"createTime":22,"updateTime":22,"relativeEntities":312,"slug":22,"properties":313,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":316,"statistic":22},[],{"title":314},{"VI":315},"The Chicago Medical School, North Chicago",[],{"title":318},{"VI":319},"Richard Wagner",{"url":303,"publisher":321,"properties":366},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":322,"slug":10,"properties":323,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":327,"manageAffiliations":340,"indexDatabases":351,"url":22,"thumbnailPath":22,"statistic":22,"gsStatistic":22,"type":22,"analyzePriority":22},[],{"issn":324,"title":325,"eissn":326},{"VOID":15},{"EN":17},{"VOID":13},[328,332,336],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":329,"label":330,"description":331,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":29},{},{"id":32,"createTime":22,"updateTime":22,"relativeEntities":333,"label":334,"description":335,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":35},{},{"id":38,"createTime":22,"updateTime":22,"relativeEntities":337,"label":338,"description":339,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":41},{},[341,346],{"id":45,"createTime":22,"updateTime":22,"relativeEntities":342,"slug":22,"properties":343,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":345,"statistic":22},[],{"title":344},{"EN":49},[51],{"id":53,"createTime":22,"updateTime":22,"relativeEntities":347,"slug":22,"properties":348,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":350,"statistic":22},[],{"title":349},{"EN":57},[51],[352,359],{"id":61,"indexDatabase":353,"url":72,"indexYears":73,"academicFieldIds":358,"indexDatabaseRanking":78},{"id":63,"createTime":22,"updateTime":22,"relativeEntities":354,"label":355,"description":356,"key":69,"publicationTags":357,"standard":22},[],{"EN":66,"VI":66},{"EN":66,"VI":68},[71],[75,76,77],{"id":80,"indexDatabase":360,"url":93,"indexYears":22,"academicFieldIds":365,"indexDatabaseRanking":22},{"id":82,"createTime":22,"updateTime":22,"relativeEntities":361,"label":362,"description":363,"key":89,"publicationTags":364,"standard":22},[],{"EN":85,"VI":85},{"EN":87,"VI":88},[91,92],[95,96],{"pages":367,"volume":369},{"VOID":368},"139-145",{"VOID":370},"2",{"total":205,"publishYear":372,"statisticByYear":373},1987,{"2009":157,"2010":143,"2011":143,"2013":143},"1987-06-01","ERROR_IN_ANALYZE_CITATION","2026-08-16T21:21:14.894+00:00",[78,91],[379,382,388,391,394,397,400,403,406],{"id":22,"text":380,"url":22,"identifiers":381},"Batson, E. (1984). Computer as consultant. Application of artificial intelligence in diagnosis.Postgrad-Med. 75(2): 211–214.",{},{"id":383,"text":384,"url":385,"identifiers":386},"4c68646b-0035-4279-8000-0006b275d4fa","Editorial (1979). Can the computer ever take over the practice of medicine?Can. Med. Assoc. J. 121: 1113.","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs10440-022-00541-7",{"doi":387},"10.1007\u002Fs10440-022-00541-7",{"id":383,"text":389,"url":385,"identifiers":390},"Korcok, M. (1985). Computer diagnostics: Technology of the future.Can. Med. Assoc. J. 133(3): 231–235.",{"doi":387},{"id":383,"text":392,"url":385,"identifiers":393},"Louria, D. B. (1981). Computers in medicine.JAMA 245(12): 1216.",{"doi":387},{"id":383,"text":395,"url":385,"identifiers":396},"Miller, R. A., Pople, H. E., Jr., and Myers, J. D. (1982). Internist-1, an experimental computer-based diagnostic consultant for general internal medicine.N. Engl. J. Med. 307(8): 468–476.",{"doi":387},{"id":383,"text":398,"url":385,"identifiers":399},"Pauker, S. G., and Kassirer, J. P. (1981). Clinical decision analysis by personal computer.Arch. Intern. Med. 141(13): 1831–1837.",{"doi":387},{"id":22,"text":401,"url":22,"identifiers":402},"Russell, S., and Uhley, H. (1983). Clinical usefulness of a personal computer (letter).JAMA 249(3): 350.",{},{"id":22,"text":404,"url":22,"identifiers":405},"Tsotsos, J. K. (1980). Can the computer ever take over the practice of medicine? (Letter).Can. Med. Assoc. J. 122(9): 993–996.",{},{"id":383,"text":407,"url":385,"identifiers":408},"Ziporyn, T. (1982). Computer-assisted medical decision-making: Interest growing (news).JAMA 248(8): 913–918.",{"doi":387},{"id":410,"createTime":411,"updateTime":412,"relativeEntities":413,"slug":414,"properties":415,"entityType":117,"verifyStatus":118,"verifyTime":426,"verifyNote":120,"languages":22,"translateLanguages":22,"viewCount":143,"primaryUrl":427,"fullTextUrl":22,"authors":428,"publicationType":233,"publisherRelationship":487,"citationCount":22,"citationInfo":22,"publishDate":538,"publishYear":539,"citationAnalyzeStatus":540,"lastCitationAnalyze":541,"indexDatabases":542,"openAccess":22,"references":22,"isForceReanalyzing":288},"a5b1b194-6a74-440c-8171-c6ff41dee5ad","2023-12-18T02:24:51.126+00:00","2026-08-15T17:42:23.352+00:00",[],"Circular-RNA-circLIFR-regulates-the-proliferation-migration-invasion-and-apoptosis-of-human-vascular-smooth-muscle-cells-via-the-miR-1299-KDR-axis",{"abstract":416,"title":418,"gsPaper":420,"references":422,"doi":424},{"EN":417},"Dysfunction of vascular smooth muscle cells (VSMCs) plays a critical role in the development of intracranial aneurysm (IA). Here, we explored the detailed role and mechanism of circular RNA (circRNA) LIF receptor subunit alpha (circLIFR, circ_0072309) in human umbilical artery smooth muscle cells (HUASMCs). CircLIFR, microRNA (miR)-1299 and kinase insert domain receptor (KDR) expression levels were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays. Cell proliferation was assessed by Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2’-Deoxyuridine (EdU) assays. Cell migration was gauged by wound-healing and transwell assays. Cell invasion and apoptosis were detected by transwell assay and flow cytometry, respectively. Direct relationship between miR-1299 and circLIFR or KDR was verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. CircLIFR and KDR were down-regulated and miR-1299 was up-regulated in the artery wall tissues and ASMCs of IA patients. Enforced expression of circLIFR enhanced HUASMC proliferation, migration, invasion, and impeded apoptosis. Mechanistically, circLIFR directly targeted miR-1299, and miR-1299 was a downstream mediator of circLIFR in regulating the proliferation, migration, invasion and apoptosis of HUASMCs. KDR was identified as a direct and functional target of miR-1299 in HUASMCs. Furthermore, circLIFR was a post-transcriptional regulator of KDR expression through miR-1299. Our findings suggest that circLIFR, an underexpressed circRNA in IA, can regulate the proliferation, migration, invasion and apoptosis of HUASMCs depending on the miR-1299\u002FKDR axis.",{"EN":419},"Circular RNA circLIFR regulates the proliferation, migration, invasion and apoptosis of human vascular smooth muscle cells via the miR-1299\u002FKDR axis",{"VOID":421},"[]",{"VOID":423},"Aoki T, Kataoka H, Nishimura M, Ishibashi R, Morishita R, Miyamoto S (2010) Ets-1 promotes the progression of cerebral aneurysm by inducing the expression of MCP-1 in vascular smooth muscle cells. Gene Ther 17:1117–1123. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fgt.2010.60\nChanakira A, Dutta R, Charboneau R, Barke R, Santilli SM, Roy S (2012) Hypoxia differentially regulates arterial and venous smooth muscle cell proliferation via PDGFR-β and VEGFR-2 expression. Am J Physiol Heart Circ Physiol 302:H1173–H1184. https:\u002F\u002Fdoi.org\u002F10.1152\u002Fajpheart.00411.2011\nChen T, Shao S, Li W, Liu Y, Cao Y (2019) The circular RNA hsa-circ-0072309 plays anti-tumour roles by sponging miR-100 through the deactivation of PI3K\u002FAKT and mTOR pathways in the renal carcinoma cell lines. Artif Cells Nanomed Biotechnol 47:3638–3648. https:\u002F\u002Fdoi.org\u002F10.1080\u002F21691401.2019.1657873\nEtminan N, Rinkel GJ (2016) Unruptured intracranial aneurysms: development, rupture and preventive management. Nat Rev Neurol 12:699–713. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnrneurol.2016.150\nGareev IF, Safin SM (2019) The role of endogenous miRNAs in the development of cerebral aneurysms. Zhurnal Voprosy Neirokhirurgii Imeni N N Burdenko 83:112–118. https:\u002F\u002Fdoi.org\u002F10.17116\u002Fneiro201983011112\nHeumüller AW, Dimmeler S (2019) Circular RNA control of vascular smooth muscle cell functions. Circ Res 124:456–458. https:\u002F\u002Fdoi.org\u002F10.1161\u002Fcircresaha.118.314521\nHou WZ, Chen XL, Wu W, Hang CH (2017) MicroRNA-370-3p inhibits human vascular smooth muscle cell proliferation via targeting KDR\u002FAKT signaling pathway in cerebral aneurysm. Eur Rev Med Pharmacol Sci 21:1080–1087\nHuang Q, Huang QY, Sun Y, Wu S (2019) High-throughput data reveals novel circular RNAs via competitive endogenous RNA networks associated with human intracranial aneurysms. Med Sci Monit 25:4819–4830. https:\u002F\u002Fdoi.org\u002F10.12659\u002Fmsm.917081\nKristensen LS, Andersen MS, Stagsted LVW, Ebbesen KK, Hansen TB, Kjems J (2019) The biogenesis, biology and characterization of circular RNAs. Nat Rev Genet 20:675–691. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fs41576-019-0158-7\nLi XG, Wang YB (2019) SRPK1 gene silencing promotes vascular smooth muscle cell proliferation and vascular remodeling via inhibition of the PI3K\u002FAkt signaling pathway in a rat model of intracranial aneurysms. CNS Neuroscience & Therapeutics 25:233–244. https:\u002F\u002Fdoi.org\u002F10.1111\u002Fcns.13043\nLi Z, Zhao R, Fang X, Huang Q, Liu J (2017) Recombinant human SDF-1α administration accelerates aneurysm neck reendothelialization in rabbit saccular aneurysm after flow diverter treatment. Acta Biochim Biophys Sin Shanghai 49:246–253. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fabbs\u002Fgmx001\nLiu D, Han L, Wu X, Yang X, Zhang Q, Jiang F (2014) Genome-wide microRNA changes in human intracranial aneurysms. BMC Neurol 14:188. https:\u002F\u002Fdoi.org\u002F10.1186\u002Fs12883-014-0188-x\nLiu X, Zhang Z, Ruan J, Pan Y, Magupalli VG, Wu H, Lieberman J (2016) Inflammasome-activated gasdermin D causes pyroptosis by forming membrane pores. Nature 535:153–158. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fnature18629\nManni S, Kisko K, Schleier T, Missimer J, Ballmer-Hofer K (2014) Functional and structural characterization of the kinase insert and the carboxy terminal domain in VEGF receptor 2 activation. FASEB J 28:4914–4923. https:\u002F\u002Fdoi.org\u002F10.1096\u002Ffj.14-256206\nMaumus-Robert S, Debette S, Bérard X, Mansiaux Y, Tubert-Bitter P, Pariente A (2020) Risk of intracranial aneurysm and dissection and fluoroquinolone use: a case-time-control study. Stroke 51:994–997. https:\u002F\u002Fdoi.org\u002F10.1161\u002Fstrokeaha.119.028490\nMeeuwsen JAL, van’t Hof FNG, van Rheenen W, GJE R, Veldink JH, Ruigrok YM (2017) Circulating microRNAs in patients with intracranial aneurysms. PLoS One 12:e0176558. https:\u002F\u002Fdoi.org\u002F10.1371\u002Fjournal.pone.0176558\nMiyata T, Minami M, Kataoka H, Hayashi K, Ikedo T, Yang T, Yamamoto Y, Yokode M, Miyamoto S (2020) Osteoprotegerin prevents intracranial aneurysm progression by promoting collagen biosynthesis and vascular smooth muscle cell proliferation. J Am Heart Assoc 9:e015731. https:\u002F\u002Fdoi.org\u002F10.1161\u002Fjaha.119.015731\nPang W, Huang F, Zhang X, Ye M, Huang Y, Huang X, Pang J, Cai C, Wang Z (2020) Circular RNA hsa_circ_0072309 inhibits non-small cell lung cancer progression by sponging miR-580-3p. Biosci Rep 40. https:\u002F\u002Fdoi.org\u002F10.1042\u002Fbsr20194237\nRivetti di Val Cervo P, Lena AM, Nicoloso M, Rossi S, Mancini M, Zhou H, Saintigny G, Dellambra E, Odorisio T, Mahé C, Calin GA, Candi E, Melino G (2012) p63-microRNA feedback in keratinocyte senescence. Proc Natl Acad Sci U S A 109:1133–1138. https:\u002F\u002Fdoi.org\u002F10.1073\u002Fpnas.1112257109\nRoviello G, Ravelli A, Fiaschi AI, Cappelletti MR, Gobbi A, Senti C, Zanotti L, Polom K, Reynolds AR, Fox SB, Generali D (2016) Apatinib for the treatment of gastric cancer. Expert Review of Gastroenterology & Hepatology 10:887–892. https:\u002F\u002Fdoi.org\u002F10.1080\u002F17474124.2016.1209407\nShibuya M (2013) Vascular endothelial growth factor and its receptor system: physiological functions in angiogenesis and pathological roles in various diseases. J Biochem 153:13–19. https:\u002F\u002Fdoi.org\u002F10.1093\u002Fjb\u002Fmvs136\nTeng L, Chen Y, Chen H, He X, Wang J, Peng Y, Duan H, Li H, Lin D, Shao B (2017) Circular RNA hsa_circ_0021001 in peripheral blood: a potential novel biomarker in the screening of intracranial aneurysm. Oncotarget 8:107125–107133. https:\u002F\u002Fdoi.org\u002F10.18632\u002Foncotarget.22349\nWang Y, Wang Y, Li Y, Wang B, Miao Z, Liu X, Ma Y (2019) Decreased expression of circ_0020397 in intracranial aneurysms may be contributing to decreased vascular smooth muscle cell proliferation via increased expression of miR-138 and subsequent decreased KDR expression. Cell Adhes Migr 13:220–228. https:\u002F\u002Fdoi.org\u002F10.1080\u002F19336918.2019.1619432\nXie C, Zhang J, Chen YE (2011) MicroRNA and vascular smooth muscle cells. Vitam Horm 87:321–339. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fb978-0-12-386015-6.00034-2\nXu Y, Yao Y, Liu Y, Wang Z, Hu Z, Su Z, Li C, Wang H, Jiang X, Kang P, Sun D, Zhong X, Cui Y (2019) Elevation of circular RNA circ_0005230 facilitates cell growth and metastasis via sponging miR-1238 and miR-1299 in cholangiocarcinoma. Aging (Albany NY) 11:1907–1917. https:\u002F\u002Fdoi.org\u002F10.18632\u002Faging.101872\nYao JS, Zhai W, Fan Y, Lawton MT, Barbaro NM, Young WL, Yang GY (2007) Interleukin-6 upregulates expression of KDR and stimulates proliferation of human cerebrovascular smooth muscle cells. J Cereb Blood Flow Metab 27:510–520. https:\u002F\u002Fdoi.org\u002F10.1038\u002Fsj.jcbfm.9600365\nYin K, Liu X (2021) Circ_0020397 regulates the viability of vascular smooth muscle cells by up-regulating GREM1 expression via miR-502-5p in intracranial aneurysm. Life Sci 265:118800. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.lfs.2020.118800\nYu Q, Dai J, Shu M (2020) Circular RNA-0072309 has antitumor influences in Hep3B cell line by targeting microRNA-665. Biofactors. https:\u002F\u002Fdoi.org\u002F10.1002\u002Fbiof.1618\nZhang L, Shao J, Zhou Y, Chen H, Qi H, Wang Y, Chen L, Zhu Y, Zhang M, Chen L, Du Y, Zhong M, Shi X, Li Q (2018) Inhibition of PDGF-BB-induced proliferation and migration in VSMCs by proanthocyanidin A2: involvement of KDR and Jak-2\u002FSTAT-3\u002FcPLA(2) signaling pathways. Biomed Pharmacother 98:847–855. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.biopha.2018.01.010\nZhang FB, Du Y, Tian Y, Ji ZG, Yang PQ (2019) MiR-1299 functions as a tumor suppressor to inhibit the proliferation and metastasis of prostate cancer by targeting NEK2. Eur Rev Med Pharmacol Sci 23:530–538. https:\u002F\u002Fdoi.org\u002F10.26355\u002Feurrev_201901_16865\nZhu H, Wang G, Zhou X, Song X, Gao H, Ma C, Chang H, Li H, Liu FF, Lu J, Ma J (2016) miR-1299 suppresses cell proliferation of hepatocellular carcinoma (HCC) by targeting CDK6. Biomed Pharmacother 83:792–797. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.biopha.2016.07.037",{"VOID":425},"10.1007\u002Fs11011-021-00853-x","2024-09-05T01:30:59.714+00:00","https:\u002F\u002Flink.springer.com\u002F10.1007\u002Fs11011-021-00853-x",[429,444,459,474],{"id":430,"sortIndex":23,"researcher":22,"roles":431,"affiliations":432,"properties":441,"displayName":443,"givenName":22,"familyName":22},"ea7cd3f2-5ff6-4355-9226-984bda5e4232",[128],[433],{"id":434,"sortIndex":23,"affiliation":435,"properties":22},"71503d97-3d4d-49fc-b09a-8c4bfa330fcb",{"id":434,"createTime":22,"updateTime":22,"relativeEntities":436,"slug":22,"properties":437,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":440,"statistic":22},[],{"title":438},{"VI":439},"Department of Nursing, Tongling Vocational and Technical College, Tongling City, China",[],{"title":442},{"VI":443},"Hui Zhang",{"id":445,"sortIndex":143,"researcher":22,"roles":446,"affiliations":447,"properties":456,"displayName":458,"givenName":22,"familyName":22},"52a96bf8-7a04-40ed-a7b4-67284702d459",[128],[448],{"id":449,"sortIndex":23,"affiliation":450,"properties":22},"34af3f8c-b980-4783-ae85-4d951f83f2f2",{"id":449,"createTime":22,"updateTime":22,"relativeEntities":451,"slug":22,"properties":452,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":455,"statistic":22},[],{"title":453},{"VI":454},"Stroke Center, Tongling People’s Hospital, Tongling, China",[],{"title":457},{"VI":458},"Bin 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effect of trophic factors on neuronal survival after 30 min oxygen and glucose deprivation (in vitro ischemia) was studied in primary hippocampal and cortical neuronal cultures of rat. In vitro ischemia was produced at 37°C by placing cultures in glucose-free medium, the oxygen content of which was removed by gassing with pure argon. After in vitro ischemia neurons were allowed to recover either in serum-free minimal essential medium (MEM) or in MEM containing 5% native horse serum, 100 ng\u002Fml basic fibroblast growth factor (bFGF) or 10 ng\u002Fml transforming growth factor-β1 (TGF-β1), respectively. Cultures that recovered in serum-free medium suffered a progressive type of neuronal injury: survival of either cortical or hippocampal neurons declined from about 60% after 1 h to 50% after 3 h, 40% after 6 h and less than 20% after 24 h. Addition of serum proteins to the incubation medium did not influence early survival (up to 3-6 h) but significantly improved survival after 24 h (more than 40% in both hippocampal and cortical cultures). Addition of TGF-β1 and bFGF had only minor effects. These data show that serum reduces delayed ischemic cell death by a mechanism which is different from that of TGF-β1 or bFGF protection.",{"EN":553},"Effect of Trophic Factors on Delayed Neuronal Death Induced by in Vitro Ischemia in Cultivated Hippocampal and Cortical Neurons",{"VOID":555},"[\"2748605125737643930\"]",{"VOID":557},"10.1023\u002FB:MEBR.0000007106.51802.37","2024-04-30T22:48:02.115+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1023\u002FB:MEBR.0000007106.51802.37",[561,576,589],{"id":562,"sortIndex":23,"researcher":22,"roles":563,"affiliations":564,"properties":573,"displayName":575,"givenName":22,"familyName":22},"9d12df2a-c200-404e-a03a-bc89cd1aa9e5",[128],[565],{"id":566,"sortIndex":23,"affiliation":567,"properties":22},"16cdcac7-c79b-43d7-ae92-7bba55bd0e2b",{"id":566,"createTime":22,"updateTime":22,"relativeEntities":568,"slug":22,"properties":569,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":572,"statistic":22},[],{"title":570},{"VI":571},"Department of Experimental Neurology, Max-Planck-Institute for Neurological Research, Cologne, Germany",[],{"title":574},{"VI":575},"M. 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(1993). In vitro model of hypoxia: basic fibroblast growth factor can rescue cultured CNS neurons from oxygen-deprived cell death. J. Cereb. Blood Flow Metab. 13:1029–1032.",{"doi":387},{"id":383,"text":674,"url":385,"identifiers":675},"Beck, T., Lindholm, D., Castren, E., and Wree, A. (1994). Brain-derived neurotrophic factor protects against ischemic cell damage in rat hippocampus. J. Cereb. Blood Flow Metab. 14:689–692.",{"doi":387},{"id":383,"text":677,"url":385,"identifiers":678},"Cheng, B., and Mattson, M.P. (1991). NGF and bFGF protect rat and human central neurons against hypoglycemic damage by stabilizing calcium homeostasis. Neuron 7:1031–1041.",{"doi":387},{"id":383,"text":680,"url":385,"identifiers":681},"Choi, D.W., Maulucci-Gedde, M., and Kriegstein, A.R. (1987). Glutamate neurotoxicity in cortical cell culture. J. Neurosci. 7:357–368.",{"doi":387},{"id":383,"text":683,"url":385,"identifiers":684},"Daval, J.-L., Ghersi-Egea, J.-F., Oillet, J., and Koziel, V. (1995). A simple method for evaluation of superoxide radical production in neural cells under various culture conditions: application to hypoxia. J. Cereb. Blood Flow Metab. 15:71–77.",{"doi":387},{"id":383,"text":686,"url":385,"identifiers":687},"Deckwerth, T.L., and Johnson, E.M.J. (1993). Temporal analysis of events associated with programmed cell death (apoptosis) of sympathetic neurons deprived of nerve growth factor. J. Cell. Biol. 123:1207–1222.",{"doi":387},{"id":689,"text":690,"url":691,"identifiers":692},"9063c441-595e-4319-b500-39f66269255a","Dux, E., Oschlies, U., Wiessner, C., and Hossmann, K.A. (1992). Glutamate-induced ribosomal disaggregation and ultrastructural-changes in rat cortical neuronal culture — protective effect of horse serum. Neurosci. Lett. 141:173–176.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F030439409290888E",{"doi":693},"10.1016\u002F0304-3940(92)90888-e",{"id":383,"text":695,"url":385,"identifiers":696},"Dux, E., Oschlies, U., Uto, A., Kusumoto, M., and Hossmann, K.-A. (1996). Early ultrastructural changes after brief histotoxic hypoxia in cultured cortical and hippocampal CA1 neurons. Acta Neuropathol. 92:541–544.",{"doi":387},{"id":383,"text":698,"url":385,"identifiers":699},"Fisher, M., Meadows, M.E., Do, T., Weise, J., Trubetskoy, V., Charette, M., and Finklestein, S.P. (1995). Delayed treatment with intravenous basic fibroblast growth factor reduces infarct size following permanent focal cerebral ischemia in rats. J. Cereb. Blood Flow Metab. 15:953–959.",{"doi":387},{"id":701,"text":702,"url":703,"identifiers":704},"e3fdb01e-4024-43d1-a55e-f198f1a18fbc","Friedrich, M., Benndorf, K., Schwalb, M., and Hirche, H. (1990). Effects of anoxia on K and Ca currents in isolated guinea pig cardiocytes. Eur. J. Physiol. 416:207–209.","http:\u002F\u002Flink.springer.com\u002F10.1007\u002FBF00370244",{"doi":705},"10.1007\u002Fbf00370244",{"id":383,"text":707,"url":385,"identifiers":708},"Goldberg, W.J., Kadingo, R.M., and Barrett, J.N. (1986). Effects of ischemia-like conditions on cultured neurons: protection by low Na+, low Ca2+ solutions. J. Neurosci. 6:3144–3151.",{"doi":387},{"id":383,"text":710,"url":385,"identifiers":711},"Gross, C.E., Howard, D.B., Dooley, R.H., Raymond, S.J., Fuller, S., and Bednar, M.M. (1994). TGF-β1 posttreatment in a rabbit model of cerebral ischaemia. Neurol. Res. 16:465–470.",{"doi":387},{"id":383,"text":713,"url":385,"identifiers":714},"Hara, H., Onodera, H., Kawagoe, J., and Kogure, K. (1991). Failure of basic fibroblast growth factor to prevent postischemic neuronal damage in the rat. Eur. J. Pharmacol. 209:195–198.",{"doi":387},{"id":383,"text":716,"url":385,"identifiers":717},"Howard, M.K., Burke, L.C., Mailhos, C., Pizzey, A., Gilbert, C.S., Lawson, W.D., et al. (1993). Cell cycle arrest of proliferating neuronal cells by serum deprivation can result in either apoptosis or differentiation. J. Neurochem. 60:1783–1791.",{"doi":387},{"id":383,"text":719,"url":385,"identifiers":720},"Iihara, K., Sasahara, M., Hashimoto, N., Uemura, Y., Kikuchi, H., and Hazama, F. (1994). Ischemia induces the expression of the platelet-derived growth factor-B chain in neurons and brain macrophages in vivo. J. Cereb. Blood Flow Metab. 14:818–824.",{"doi":387},{"id":383,"text":722,"url":385,"identifiers":723},"Kaku, D.A., Giffard, R.G., and Choi, D.W. (1993). Neuroprotective effects of glutamate antagonists and extracellular acidity. Science 260:1516–1518.",{"doi":387},{"id":383,"text":725,"url":385,"identifiers":726},"Kohmura, E., Yamada, K., Hayakawa, T., Kinoshita, A., Matsumoto, K., and Mogami, H. (1990). Hippocampal neurons become more vulnerable to glutamate after subcritical hypoxia: an in vitro study. J. Cereb. Blood Flow Metab. 10:877–884.",{"doi":387},{"id":383,"text":728,"url":385,"identifiers":729},"Kokaia, Z., Zhao, Q., Kokaia, M., Elmer, E., Metsis, M., Smith, M.-L., et al. (1995). Regulation of brain-derived neurotrophic factor gene expression after transient middle cerebral artery occlusion with and without brain damage. Exp. Neurol. 136:73–88.",{"doi":387},{"id":383,"text":731,"url":385,"identifiers":732},"Koketsu, N., Berlove, D.J., Moskowitz, M.A., Kowall, N.W., Caday, C.G., and Finklestein, S.P. (1994). Pretreatment with intraventricular basic fibroblast growth factor decreases infarct size following focal cerebral ischemia in rats. Ann. Neurol. 35:451–457.",{"doi":387},{"id":383,"text":734,"url":385,"identifiers":735},"Kusumoto, M., Arai, H., Mori, K., and Sato, K. (1995). Resistance to cerebral ischemia in developing gerbils. J. Cereb. Blood Flow Metab. 15:886–891.",{"doi":387},{"id":383,"text":737,"url":385,"identifiers":738},"Kusumoto, M., Dux, E., Paschen, W., and Hossmann, K.-A. (1996). Susceptibility of hippocampal and cortical neurons to argon-mediated in vitro ischemia. J. Neurochem. 67:1613–1621.",{"doi":387},{"id":383,"text":740,"url":385,"identifiers":741},"Lee, W.H., Wang, G.M., Seaman, L.B., and Vannucci, S.J. (1996). Coordinate IGF-I and IGFBP5 gene expression in perinatal rat brain after hypoxia-ischemia. J. Cereb. Blood Flow Metab. 16:227–236.",{"doi":387},{"id":383,"text":743,"url":385,"identifiers":744},"Lindvall, O., Ernfors, P., Bengzon, J., Kokaia, Z., Smith, M.-L., Siesjö, B.K., and Persson, H. (1992). Differential regulation of mRNAs for nerve growth factor, brain-derived neurotrophic factor, and neurotrophin 3 in the adult rat brain following cerebral ischemia and hypoglycemic coma. Proc. Natl. Acad. Sci. USA. 89:648–652.",{"doi":387},{"id":383,"text":746,"url":385,"identifiers":747},"Linnik, M.D., Zobrist, R.H., and Hatfield, M.D. (1993). Evidence supporting a role for programmed cell death in focal cerebral ischemia in rats. Stroke. 24:2002–2008.",{"doi":387},{"id":749,"text":750,"url":751,"identifiers":752},"f5d788e9-536d-4976-80ce-5eb2aac384dc","Lobner, D., and Choi, D.W. (1996). Preincubation with protein synthesis inhibitors protects cortical neurons against oxygen-glucose deprivation-induced death. Neuroscience. 72:335–341.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F0306452295005617",{"doi":753},"10.1016\u002F0306-4522(95)00561-7",{"id":383,"text":755,"url":385,"identifiers":756},"MacMillan, V., Walton-Roche, K., and Davis, J. (1993). Acidic fibroblast growth factor infusion reduces ischemic CA1 hippocampal damage in the gerbil. Can. J. Neurol. Sci. 20:37–40.",{"doi":387},{"id":22,"text":758,"url":22,"identifiers":759},"Martinez, H., Cahn, R., Mrsulja, B.B., and Klatzo, I. (1984). Reactivity of young gerbil brain to cerebral ischemia. J. Neuropathol. Exp. Neurol. 43:352–352.",{},{"id":383,"text":761,"url":385,"identifiers":762},"Martinou, J., Dubois-Dauphin, M., Staple, J.K., Rodrigues, I., Frankowski, H., Missoten, M., et al. (1994). Overexpression of BCL-2 in transgenic mice protects neurons from naturally occurring cell death and experimental ischemia. Neuron 13:1017–1030.",{"doi":387},{"id":383,"text":764,"url":385,"identifiers":765},"Pechan, P.A., Yoshida, T., Panahian, N., Moskowitz, M.A., and Breakefield, X.O. (1995). Genetically modified fibroblasts producing NGF protect hippocampal neurons after ischemia in the rat. NeuroReport. 6:669–672.",{"doi":387},{"id":383,"text":767,"url":385,"identifiers":768},"Pittmann, R.N., Wang, S., DiBenedetto, A.J., and Mills, J.C. (1993). A system for characterizing cellular and molecular events in programmed neuronal cell death. J. Neurosci. 13:3669–3680.",{"doi":387},{"id":383,"text":770,"url":385,"identifiers":771},"Prehn, J.H.M., Backhaub, C., and Krieglstein, J. (1993). Transforming growth factor-β1 prevents glutamate neurotoxicity in rat neocortical cultures and protects mouse neocortex from ischemic injury in vivo. J. Cereb. Blood Flow Metab. 13:521–525.",{"doi":387},{"id":773,"text":774,"url":775,"identifiers":776},"623e7763-2dea-49a2-b593-a43d0e603b11","Regan, R.F., Panter, S.S., With, A., Tilly, J.L., and Giffard, R.G. (1995). Ultrastructure of excitotoxic neuronal death in murine cortical culture. Brain Res. 705:188–198.","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002F0006899395011706",{"doi":777},"10.1016\u002F0006-8993(95)01170-6",{"id":383,"text":779,"url":385,"identifiers":780},"Rosenbaum, D.M., Michaelson, M., Batter, D.K., Doshi, P., and Kessler, J.A. (1994). Evidence for hypoxia-induced, programmed cell death of cultured neurons. Ann. Neurol. 36:864–870.",{"doi":387},{"id":383,"text":782,"url":385,"identifiers":783},"Rosenblatt, S., Irikura, K., Caday, C.G., Finklestein, S.P., and Moskowitz, M.A. (1994). Basic fibroblast growth factor dilates rat pial arterioles. J. Cereb. Blood Flow Metab. 14:70–74.",{"doi":387},{"id":785,"text":786,"url":787,"identifiers":788},"9183a4ae-15d7-419e-8769-403043bdaeef","Shuaib, A., Sochocka, E., Ishaqzay, R., Hertz, L., and Code, W.E. (1993). Protective effect of hypothermia during ischemia in neural cell cultures. Neurochem. Res. 18:663–665.","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF00966779",{"doi":789},"10.1007\u002FBF00966779",{"id":383,"text":791,"url":385,"identifiers":792},"Tanaka, R., Miyasaka, Y., Yada, K., Ohwada, T., and Kameya, T. (1995). Basic fibroblast growth factor increases regional cerebral blood flow and reduces infarct size after experimental ischemia in a rat model. Stroke. 26:2154–2158.",{"doi":387},{"id":383,"text":794,"url":385,"identifiers":795},"Uto, A., Dux, E., and Hossmann, K.-A. (1994). Effect of serum on intracellular calcium homeostasis and survival of primary cortical and hippocampal CA1 neurons following brief glutamate treatment. Metab. Brain Dis. 9:333–345.",{"doi":387},{"id":383,"text":797,"url":385,"identifiers":798},"Uto, A., Dux, E., Kusumoto, M., and Hossmann, K.-A. (1995). Delayed neuronal death after brief histotoxic hypoxia in vitro. J. Neurochem. 64:2185–2192.",{"doi":387},{"id":383,"text":800,"url":385,"identifiers":801},"Yamashita, K., Wiessner, C., Lindholm, D., Thoenen, H., and Hossmann, K.-A. (1997). Post-occlusion treatment with BDNF reduces infarct size in a model of permanent occlusion of the middle cerebral artery in rats. (Submitted).",{"doi":387},{"id":803,"createTime":804,"updateTime":805,"relativeEntities":806,"slug":807,"properties":808,"entityType":117,"verifyStatus":118,"verifyTime":819,"verifyNote":120,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":820,"fullTextUrl":22,"authors":821,"publicationType":233,"publisherRelationship":852,"citationCount":903,"citationInfo":904,"publishDate":911,"publishYear":905,"citationAnalyzeStatus":21,"lastCitationAnalyze":912,"indexDatabases":913,"openAccess":22,"references":22,"isForceReanalyzing":288},"16733a4a-9194-43b7-81d9-b1e662d9fda8","2023-12-23T07:39:38.276+00:00","2026-07-27T09:45:39.757+00:00",[],"Electromagnetic-radiation-Wi-Fi-and-epilepsy-induce-calcium-entry-and-apoptosis-through-activation-of-TRPV1-channel-in-hippocampus-and-dorsal-root-ganglion-of-rats",{"abstract":809,"title":811,"gsPaper":813,"references":815,"doi":817},{"EN":810},"Incidence rates of epilepsy and use of Wi-Fi worldwide have been increasing. TRPV1 is a Ca2+ permeable and non-selective channel, gated by noxious heat, oxidative stress and capsaicin (CAP). The hyperthermia and oxidant effects of Wi-Fi may induce apoptosis and Ca2+ entry through activation of TRPV1 channel in epilepsy. Therefore, we tested the effects of Wi-Fi (2.45 GHz) exposure on Ca2+ influx, oxidative stress and apoptosis through TRPV1 channel in the murine dorsal root ganglion (DRG) and hippocampus of pentylentetrazol (PTZ)-induced epileptic rats. Rats in the present study were divided into two groups as controls and PTZ. The PTZ groups were divided into two subgroups namely PTZ + Wi-Fi and PTZ + Wi-Fi + capsazepine (CPZ). The hippocampal and DRG neurons were freshly isolated from the rats. The DRG and hippocampus in PTZ + Wi-Fi and PTZ + Wi-Fi + CPZ groups were exposed to Wi-Fi for 1 hour before CAP stimulation. The cytosolic free Ca2+, reactive oxygen species production, apoptosis, mitochondrial membrane depolarization, caspase-3 and −9 values in hippocampus were higher in the PTZ group than in the control although cell viability values decreased. The Wi-Fi exposure induced additional effects on the cytosolic Ca2+ increase. However, pretreatment of the neurons with CPZ, results in a protection against epilepsy-induced Ca2+ influx, apoptosis and oxidative damages. In results of whole cell patch-clamp experiments, treatment of DRG with Ca2+ channel antagonists [thapsigargin, verapamil + diltiazem, 2-APB, MK-801] indicated that Wi-Fi exposure induced Ca2+ influx via the TRPV1 channels. In conclusion, epilepsy and Wi-Fi in our experimental model is involved in Ca2+ influx and oxidative stress-induced hippocampal and DRG death through activation of TRPV1 channels, and negative modulation of this channel activity by CPZ pretreatment may account for the neuroprotective activity against oxidative stress.",{"EN":812},"Electromagnetic radiation (Wi-Fi) and epilepsy induce calcium entry and apoptosis through activation of TRPV1 channel in hippocampus and dorsal root ganglion of rats",{"VOID":814},"[\"4676201670789377343\"]",{"VOID":816},"Adey WR, Bawin SM, Lawrence AF (1982) Effects of weak amplitude-modulated microwave fields on calcium efflux from awake cat cerebral cortex. Bioelectromagnetics 3:295–307\nAït-Aïssa S, Billaudel B, Poulletier de Gannes F, Ruffié G, Duleu S, Hurtier A, Haro E, Taxile M, Athané A, Geffard M, Wu T, Wiart J, Bodet D, Veyret B, Lagroye I (2012) In utero and early-life exposure of rats to a Wi-Fi signal: screening of immune markers in sera and gestational outcome. Bioelectromagnetics 33:410–420\nAmmari M, Lecomte A, Sakly M, Abdelmelek H, de-Seze R (2008) Exposure to GSM 900 MHz electromagnetic fields affects cerebral cytochrome c oxidase activity. Toxicology 250(1):70–74\nBawin SM, Adey WR, Sabbot IM (1978) Ionic factors in release of 45Ca2+ from chicken cerebral tissue by electromagnetic fields. Proc Natl Acad Sci U S A 75(12):6314–6318\nBerman E, Carter HB, House D (1981) Observations of rat fetuses after irradiation with 2450 MHz (CW) microwaves. J Microw Power 16:9–13\nBerman E, Carter HB, House D (1982) Observations of Syrian hamster fetuses after exposure to 2450-MHz microwaves. J Microw Power 17:107–112\nBhaskaran MD, Smith BN (2010) Effects of TRPV1 activation on synaptic excitation in the dentate gyrus of a mouse model of temporal lobe epilepsy. Exp Neurol 223:529–536\nBurkhardt M, Pokovic K, Gnos M, Schmid T, Kuster N (1996) Numerical and experimental dosimetry of petri dish exposure setups. Bioelectromagnetics 17:483–493\nCarballo-Quintás M, Martínez-Silva I, Cadarso-Suárez C, Alvarez-Figueiras M, Ares-Pena FJ, López-Martín E (2011) A study of neurotoxic biomarkers, c-fos and GFAP after acute exposure to GSM radiation at 900 MHz in the picrotoxin model of rat brains. Neurotoxicology 32:478–494\nCelik O, Nazıroğlu M (2012) Melatonin modulates apoptosis and TRPM2 channels in transfected cells activated by oxidative stress. Physiol Behav 107:458–465\nDasdag S, Akdag MZ, Ulukaya E, Uzunlar AK, Ocak AR (2009) Effect of mobile phone exposure on apoptotic glial cells and status of oxidative stress in rat brain. 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Toxicol Ind Health 22:211–216\nManikonda PK, Rajendra P, Devendranath D, Gunasekaran B, Channakeshava ARS, Sashidhar RB, Subramanyam C (2007) Influence of extremely low frequency magnetic fields on Ca2+ signaling and NMDA receptor functions in rat hippocampus. Neurosci Lett 413:145–149\nManna SS, Umathe SN (2012) Involvement of transient receptor potential vanilloid type 1 channels in the pro-convulsant effect of anandamide in pentylenetetrazole-induced seizures. Epilepsy Res 100:113–124\nMeldrum BS (2002) Concept of activity-induced cell death in epilepsy: historical and contemporary perspectives. Prog Brain Res 135:3–11\nMelnikova VO, Ananthaswamy HN (2005) Cellular and molecular events leading to the development of skin cancer. Mutat Res 571:91–106\nNazıroğlu M (2009) Role of selenium on calcium signaling and oxidative stress-induced molecular pathways in epilepsy. Neurochem Res 34:2181–2191\nNazıroğlu M (2012) Molecular role of catalase on oxidative stress-induced Ca(2+) signaling and TRP cation channel activation in nervous system. J Recept Signal Transduct Res 32:134–141\nNazıroğlu M, Akman H. (2014) Effects of cellular phone and Wi-Fi-induced electromagnetic radiation on oxidative stress and molecular pathways in brain. I. Laher (ed.), Systems Biology of Free Radicals and Anti-Oxidants. Springer-Verlag Berlin Heidelberg DOI 10.1007\u002F978-3-642-30018-9_210\nNazıroğlu M, Gümral N (2009) Modulator effects of L-carnitine and selenium on wireless devices (2.45 GHz)-induced oxidative stress and electroencephalography records in brain of rat. Int J Radiat Biol 85:680–689\nNazıroğlu M, Tokat S, Demirci S (2012a) Role of melatonin on electromagnetic radiation-induced oxidative stress and Ca2+ signaling molecular pathways in breast cancer. J Recept Signal Transduct Res 32:290–297\nNazıroğlu M, Çelik Ö, Özgül C, Doğan S, Bal R, Gümral N, Rodríguez AB, Pariente JA (2012b) Melatonin modulates wireless devices (2.45 GHz)-induced brain and dorsal root ganglion injury through TRPM2 and voltage gated calcium channels in rat. Physiol Behav 105:683–692\nNazıroğlu M, Ciğ B, Doğan S, Uğuz AC, Dilek S, Faouzi D (2012c) 2.45-GHz wireless devices induce oxidative stress and proliferation through cytosolic Ca2+ influx in human leukemia cancer cells. Int J Radiat Biol 88:449–456\nNazıroğlu M, Dikici DM, Dursun S (2012d) Role of oxidative stress and Ca(2+) signaling on molecular pathways of neuropathic pain in diabetes: Focus on TRP channels. Neurochem Res 37:2065–2075\nNazıroğlu M, Çiğ B, Özgül C (2013a) Neuroprotection induced by N-acetylcysteine against cytosolic glutathione depletion induced-Ca2+ influx in dorsal root ganglion neurons of mice: Role of TRPV1 channels. Neuroscience 242:151–160\nNazıroğlu M, Akay MB, Celik O, Yıldırım MI, Balcı E, Yürekli VA (2013b) Capparis ovata Modulates Brain Oxidative Toxicity and Epileptic Seizures in Pentylentetrazol-Induced Epileptic Rats. Neurochem Res 38:780–788\nNazıroğlu M, Ciğ B, Ozgül C (2014) Modulation of oxidative stress and Ca(2+) mobilization through TRPM2 channels in rat dorsal root ganglion neuron by Hypericum perforatum. Neuroscience 28(263):27–35\nO’Connor RP, Madison SD, Leveque P, Roderick HL, Bootman MD (2010) Exposure to GSM RF fields does not affect calcium homeostasis in human endothelial cells, rat pheocromocytoma cells or rat hippocampal neurons. PLoS One 27(5):e11828\nPiacentini R, Ripoli C, Mezzogori D, Azzena GB, Grassi C (2008) Extremely low-frequency electromagnetic fields promote in vitro neurogenesis via upregulation of Ca(v)1-channel activity. 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J Mol Neurosci 49:182–193\nSusankova K, Tousova K, Vyklicky L, Teisinger J, Vlachova V (2006) Reducing and oxidizing agents sensitize heat-activated vanilloid receptor (TRPV1) current. Mol Pharmacol 70:383–394\nTjiattas L, Ortiz DO, Dhivant S, Mitton K, Rogers E, Shea TB (2004) Folate deficiency and homocysteine induce toxicity in cultured dorsal root ganglion neurons via cytosolic calcium accumulation. Aging Cell 3:71–76\nUğuz AC, Nazıroğlu M (2012) Effects of selenium on calcium signaling and apoptosis in rat dorsal root ganglion neurons induced by oxidative stress. Neurochem Res 37:1631–1638\nUğuz AC, Nazıroğlu M, Espino J, Bejarano I, González D, Rodríguez AB, Pariente JA (2009) Selenium modulates oxidative stress-induced cell apoptosis in human myeloid HL-60 cells via regulation of caspase-3,−9 and calcium influx. J Membr Biol 232:15–23\nUğuz AC, Cig B, Espino J, Bejarano I, Nazıroğlu M, Rodríguez AB, Pariente JA (2012) Melatonin potentiates chemotherapy-induced cytotoxicity and apoptosis in rat pancreatic tumor cells. J Pineal Res 53:91–98\nYang XS, He GL, Hao YT, Xiao Y, Chen CH, Zhang GB, Yu ZP (2012) Exposure to 2.45 GHz electromagnetic fields elicits an HSP-related stress response in rat hippocampus. Brain Res Bull 88:371–378\nZhao R, Zhang S, Xu Z, Ju L, Lu D, Yao G (2007) Studying gene expression profile of rat neuron exposed to 1800MHz radiofrequency electromagnetic fields with cDNA microassay. Toxicology 25(235):167–175\nZhou XR, Yuan HP, Qu W, Ma CY, Li HY, Wang Y (2008) The study of retinal ganglion cell apoptosis induced by different intensities of microwave irradiation. Ophthalmologica 222:6–10",{"VOID":818},"10.1007\u002Fs11011-014-9549-9","2024-09-21T09:02:03.433+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11011-014-9549-9",[822,837],{"id":823,"sortIndex":23,"researcher":22,"roles":824,"affiliations":825,"properties":834,"displayName":836,"givenName":22,"familyName":22},"ed6acfe9-1319-4fac-b541-8c3eced38262",[128],[826],{"id":827,"sortIndex":23,"affiliation":828,"properties":22},"13f2cb45-8549-41bd-8262-6de4c3901eca",{"id":827,"createTime":22,"updateTime":22,"relativeEntities":829,"slug":22,"properties":830,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":833,"statistic":22},[],{"title":831},{"VI":832},"Neuroscience Research Center, University of Suleyman Demirel, Isparta, Turkey",[],{"title":835},{"VI":836},"Vahid Ghazizadeh",{"id":838,"sortIndex":143,"researcher":22,"roles":839,"affiliations":840,"properties":847,"displayName":849,"givenName":22,"familyName":22},"94139543-5ad2-459a-8821-31408d91e375",[128],[841],{"id":827,"sortIndex":23,"affiliation":842,"properties":22},{"id":827,"createTime":22,"updateTime":22,"relativeEntities":843,"slug":22,"properties":844,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":846,"statistic":22},[],{"title":845},{"VI":832},[],{"title":848,"gsAuthor":850},{"VI":849},"Mustafa Nazıroğlu",{"VOID":851},"[\"QLJOb7IAAAAJ\"]",{"url":820,"publisher":853,"properties":898},{"id":6,"createTime":7,"updateTime":8,"relativeEntities":854,"slug":10,"properties":855,"entityType":20,"verifyStatus":21,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":23,"subjectFields":859,"manageAffiliations":872,"indexDatabases":883,"url":22,"thumbnailPath":22,"statistic":22,"gsStatistic":22,"type":22,"analyzePriority":22},[],{"issn":856,"title":857,"eissn":858},{"VOID":15},{"EN":17},{"VOID":13},[860,864,868],{"id":26,"createTime":22,"updateTime":22,"relativeEntities":861,"label":862,"description":863,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":29},{},{"id":32,"createTime":22,"updateTime":22,"relativeEntities":865,"label":866,"description":867,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":35},{},{"id":38,"createTime":22,"updateTime":22,"relativeEntities":869,"label":870,"description":871,"parentId":22,"standard":22,"scholarHubFieldId":22},[],{"EN":41},{},[873,878],{"id":45,"createTime":22,"updateTime":22,"relativeEntities":874,"slug":22,"properties":875,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":877,"statistic":22},[],{"title":876},{"EN":49},[51],{"id":53,"createTime":22,"updateTime":22,"relativeEntities":879,"slug":22,"properties":880,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":882,"statistic":22},[],{"title":881},{"EN":57},[51],[884,891],{"id":61,"indexDatabase":885,"url":72,"indexYears":73,"academicFieldIds":890,"indexDatabaseRanking":78},{"id":63,"createTime":22,"updateTime":22,"relativeEntities":886,"label":887,"description":888,"key":69,"publicationTags":889,"standard":22},[],{"EN":66,"VI":66},{"EN":66,"VI":68},[71],[75,76,77],{"id":80,"indexDatabase":892,"url":93,"indexYears":22,"academicFieldIds":897,"indexDatabaseRanking":22},{"id":82,"createTime":22,"updateTime":22,"relativeEntities":893,"label":894,"description":895,"key":89,"publicationTags":896,"standard":22},[],{"EN":85,"VI":85},{"EN":87,"VI":88},[91,92],[95,96],{"pages":899,"volume":901},{"VOID":900},"787-799",{"VOID":902},"29",80,{"total":903,"publishYear":905,"statisticByYear":906},2014,{"2014":205,"2015":907,"2016":221,"2017":189,"2018":908,"2019":909,"2020":908,"2021":910,"2022":189,"2023":189,"2024":189,"2025":189,"2026":173},12,8,7,11,"2014-05-03","2026-07-27T09:45:39.756+00:00",[78,91],{"id":915,"createTime":916,"updateTime":917,"relativeEntities":918,"slug":919,"properties":920,"entityType":117,"verifyStatus":118,"verifyTime":931,"verifyNote":120,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":932,"fullTextUrl":22,"authors":933,"publicationType":233,"publisherRelationship":1018,"citationCount":22,"citationInfo":22,"publishDate":1069,"publishYear":1070,"citationAnalyzeStatus":375,"lastCitationAnalyze":1071,"indexDatabases":1072,"openAccess":22,"references":22,"isForceReanalyzing":288},"dc80bf99-3cd6-40ce-815a-2a8fdc97f87f","2024-01-16T00:57:40.339+00:00","2026-07-23T14:46:47.696+00:00",[],"Liver-transplantation-and-neurological-side-effects",{"abstract":921,"title":923,"gsPaper":925,"references":927,"doi":929},{"EN":922},"Advances in liver transplantation (LT), particularly in immunosuppression and intensive care treatment have had increased the number of long-term survivors following liver transplantation. In order of more long-term survivors, reports about neurological complication following liver transplantation are increasing. Neurological complications are not uncommon in liver transplant recipients, which contribute to a longer ICU- and in-hospital stay. Every effort should be focused on early detection to prevent the patient from this life-threatening event, which is often associated with poor life quality.",{"EN":924},"Liver transplantation and neurological side effects",{"VOID":926},"[\"13734747513909980220\"]",{"VOID":928},"Adams DH et al (1987) Neurological complications following liver transplantation. Lancet 1:949–951\nEstol CJ et al (1989) Seizures after liver transplantation: a clinicopathologic study. Neurology 39:1297–1301\nFerreiro JA et al (1992) Neuropathologic findings after liver transplantation. Acta Neuropathol (Berl) 84:1–14\nFreise CE et al (1991) Similar clinical presentation of neurotoxicity following FK 506 and cyclosporine in a liver transplant recipient. Transplant Proc 23:3173–3174\nFruhauf NR et al (2003) Late onset of tacrolimus-related posterior leukoencephalopathy after living donor liver transplantation. Liver Transpl 9:983–985\nGhaus N et al (2001) Neurological complications in liver transplantation. J Neurol 248:1042–1048\nHinchey J et al (1996) A reversible posterior leukoencephalopathy syndrome. N Engl J Med 334:494–500\nKim BS et al (2007) Neurologic complications in adult living donor liver transplant recipients. Clin Transplant 21:544–547\nLewis MB, Howdle PD (2003) Neurologic complications of liver transplantation in adults. Neurology 61:1174–1178\nMartinez AJ (1998) The neuropathology of organ transplantation: comparison and contrast in 500 patients. Pathol Res Pract 194:473–486\nMenegaux F et al (1994) Neurological complications of liver transplantation in adult versus pediatric patients. Transplantation 58:447–450\nMcDiarmid SV et al (1995) FK506 (tacrolimus) compared with cyclosporine for primary immunosuppression after pediatric liver transplantation. Results from the U.S. Multicenter Trial. Transplantation 59:530–536\nMoreno E et al (1993) Neurologic complications in liver transplantation. Acta Neurol Scand 87:25–31\nMueller AR et al (1994) Neurotoxicity after orthotopic liver transplantation. A comparison between cyclosporine and FK506. Transplantation 58:155–170\nPujol A et al (1994) Predictive factors of in-hospital CNS complications following liver transplantation. Neurology 44:1226–1230\nSaner F et al (2006) Neurological complications after cadaveric and living donor liver transplantation. J Neurol 253:612–617\nSaner FH et al (2007) Severe neurological events following liver transplantation. Arch Med Res 38:75–79\nSommer BG et al (1985) Cyclosporine-associated renal arteriopathy resulting in loss of allograft function. Am J Surg 149:756–764\nStarzl TE et al (1965) Clinical experience with organ transplantation. South Med J 58:131–147\nStarzl TE et al (1985) Refinements in the surgical technique of liver transplantation. Semin Liver Dis 5:349–56\nStein DP et al (1992) Neurological complications following liver transplantation. Ann Neurol 31:644–649\nStracciari A, Guarino M (2001) Neuropsychiatric complications of liver transplantation. Metab Brain Dis 16:3–11\nVogt DP et al (1988) Neurologic complications of liver transplantation. Transplantation 45:1057–1061\nWijdicks EF et al (1994) FK506-induced neurotoxicity in liver transplantation. Ann Neurol 35:498–501\nWijdicks EF et al (1996) Causes and outcome of seizures in liver transplant recipients. Neurology 47:1523–1525",{"VOID":930},"10.1007\u002Fs11011-008-9119-0","2024-06-25T07:01:19.582+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11011-008-9119-0",[934,951,966,979,992,1005],{"id":935,"sortIndex":23,"researcher":22,"roles":936,"affiliations":937,"properties":946,"displayName":948,"givenName":22,"familyName":22},"730b7a4d-b5b9-4a07-89c3-eb94b126d3f8",[128],[938],{"id":939,"sortIndex":23,"affiliation":940,"properties":22},"548aceb3-9161-4ac4-bb34-82becd6c1ecf",{"id":939,"createTime":22,"updateTime":22,"relativeEntities":941,"slug":22,"properties":942,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":945,"statistic":22},[],{"title":943},{"VI":944},"Department of General-, Visceral and Transplant Surgery, University Hospital Essen, Essen, Germany",[],{"title":947,"gsAuthor":949},{"VI":948},"Fuat H. 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Hepatol Res 21:199–204",{"doi":387},{"id":1498,"createTime":1499,"updateTime":1500,"relativeEntities":1501,"slug":1502,"properties":1503,"entityType":117,"verifyStatus":118,"verifyTime":1513,"verifyNote":120,"languages":22,"translateLanguages":22,"viewCount":23,"primaryUrl":1514,"fullTextUrl":22,"authors":1515,"publicationType":233,"publisherRelationship":1656,"citationCount":22,"citationInfo":22,"publishDate":1705,"publishYear":286,"citationAnalyzeStatus":540,"lastCitationAnalyze":1706,"indexDatabases":1707,"openAccess":22,"references":22,"isForceReanalyzing":288},"0da9e0a6-f40e-43da-815f-aa88dea0e5f5","2023-12-28T11:37:04.586+00:00","2026-07-20T20:04:37.893+00:00",[],"Molecular-dynamics-exploration-of-Lupenone-therapeutic-implications-for-glioblastoma-multiforme-and-alzheimer-s-amyloid-beta-pathogenesis",{"abstract":1504,"title":1506,"gsPaper":1508,"references":1509,"doi":1511},{"EN":1505},"Neuro-oncological and neurodegenerative disorders, represented paradigmatically by glioblastoma and Alzheimer's disease, respectively, persist as formidable challenges in the biomedical realm. The interconnected molecular underpinnings of these conditions necessitate rigorous and novel therapeutic examinations. This comprehensive research was anchored on the premise of unveiling the therapeutic potential and specificity of Lupenone, a potent phytoconstituent, in targeting the molecular pathways underpinning both glioblastoma and Alzheimer's amyloid beta pathology. This was gauged through its interactions with key protein structures, 5H08 and 2ZHV. An integrative approach was adopted, marrying advanced proteomics and modern computer-aided drug design techniques. Molecular docking of Lupenone with 5H08 and 2ZHV was meticulously executed, with subsequent molecular dynamics simulations providing insights into the stability, viability, and intricacies of these interactions. Lupenone demonstrated profound binding affinities, evidenced by robust docking scores of -9.54 kcal\u002Fmol for 5H08 and -10.59 kcal\u002Fmol for 2ZHV. These interactions underscored Lupenone's eminent therapeutic potential in mitigating glioblastoma and modulating the amyloid beta pathology inherent to Alzheimer's. The introduction of Proteolysis Targeting Chimeras (PROTACs) further magnified the therapeutic prospects, accentuating Lupenone's efficacy. The findings of this study not only underscore the therapeutic acumen of Lupenone in addressing the challenges posed by glioblastoma and Alzheimer's but also lay a strong foundation for its consideration as a leading candidate in future neuro-oncological and neurodegenerative research endeavors. Given the compelling in-silico data, a clarion call is made for its empirical validation in holistic in-vivo settings, potentially pioneering a new therapeutic epoch in both glioblastoma and Alzheimer's interventions.",{"EN":1507},"Molecular dynamics exploration of Lupenone: therapeutic implications for glioblastoma multiforme and alzheimer's amyloid beta pathogenesis",{"VOID":421},{"VOID":1510},"Atkinson GP, Nozell SE, Benveniste ETN (2010) NF-κB and STAT3 signaling in glioma: targets for future therapies. Expert Rev Neurother 10(4):575–586\nAtiq A, Parhar I (2020) Anti-neoplastic potential of flavonoids and polysaccharide phytochemicals in glioblastoma. Molecules 25(21):4895\nBékés M, Langley DR, Crews CM (2022) PROTAC targeted protein degraders: the past is prologue. 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Front Mol Biosci 7:193",{"VOID":1512},"10.1007\u002Fs11011-023-01319-y","2024-06-26T05:22:56.318+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs11011-023-01319-y",[1516,1531,1546,1561,1574,1589,1602,1617,1632],{"id":1517,"sortIndex":23,"researcher":22,"roles":1518,"affiliations":1519,"properties":1528,"displayName":1530,"givenName":22,"familyName":22},"0d09a0d7-55f8-4141-b047-836e95e55cc3",[128],[1520],{"id":1521,"sortIndex":23,"affiliation":1522,"properties":22},"524f23c2-bb9e-4813-a7f3-2d7c50255912",{"id":1521,"createTime":22,"updateTime":22,"relativeEntities":1523,"slug":22,"properties":1524,"entityType":22,"verifyStatus":22,"verifyTime":22,"verifyNote":22,"languages":22,"translateLanguages":22,"viewCount":22,"url":22,"parentIds":1527,"statistic":22},[],{"title":1525},{"EN":1526},"Department of Basic Science, College of Medicine, Princess Nourah bint Abdulrahman University, Riyadh, Saudi Arabia",[],{"title":1529},{"VI":1530},"Hailah M. 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Despite considerable recent advances in the treatment of ischemic stroke, only a limited number of effective neuroprotective agents are available for stroke. Green tea (Camellia sinensis) is a popular herbal plant, and numerous studies have indicated its health benefits for several diseases. Green tea is of interest due to its high content of catechin derivatives, including epicatechin, gallocatechin, epicatechin gallate, epigallocatechin, and epigallocatechin-3-gallate. This review tried to develop a feasible background for the potential effects of green tea and its bioactive derivatives concerning protection against ischemic stroke. Green tea’s antioxidants, anti-inflammatory, anti-apoptotic, and neuroprotective effects are believed to be efficacious in stroke treatment. Evidence supports the idea that green tea can be used to assist in treating ischemic stroke. \n                \n                  \n                    \n                  \n                \n               Green tea has a protective effect against ischemic stroke; Epigallocatechin-3-gallate: EGCG, Epicatechin: EC, Gallocatechin gallate: GCG, Epigallocatechin: EGC, Epicatechin gallate: ECG, Catechin: C, Gallocatechin: GC.",{"EN":1718},"Therapeutic potentialities of green tea (Camellia sinensis) in ischemic stroke: biochemical and molecular 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Behav Brain Res 321:79–86. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.bbr.2016.12.037","https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.bbr.2016.12.037",{"mag":1852,"openalex":1853,"pm":1854,"doi":1855},"2562798178","W2562798178","28042007","10.1016\u002Fj.bbr.2016.12.037",{"id":1857,"text":1858,"url":1859,"identifiers":1860},"94048021-db76-4f37-b786-7aa3df7adc56","Barthels D, Das H (2020) Current advances in ischemic stroke research and therapies Biochimica et Biophysica Acta (BBA) - molecular basis. https:\u002F\u002Fdoi.org\u002F10.1016\u002Fj.bbadis.2018.09.012. of Disease 1866:165260 doi","https:\u002F\u002Fwww.sciencedirect.com\u002Fscience\u002Farticle\u002Fpii\u002FS0925443918303478",{"doi":1861},"10.1016\u002Fj.bbadis.2018.09.012",{"id":22,"text":1863,"url":22,"identifiers":1864},"Bedrood Z, Rameshrad M, Hosseinzadeh H (2018) Toxicological effects of Camellia sinensis (green tea): a review. Phytother Res 32:1163–1180",{},{"id":383,"text":1866,"url":385,"identifiers":1867},"Bernatoniene J, Kopustinskiene DM (2018a) The role of catechins in cellular responses to oxidative stress Molecules 23:965",{"doi":387},{"id":22,"text":1869,"url":1870,"identifiers":1871},"Bernatoniene J, Kopustinskiene DM (2018b) The role of catechins in Cellular responses to oxidative stress molecules. 23. https:\u002F\u002Fdoi.org\u002F10.3390\u002Fmolecules23040965","https:\u002F\u002Fdoi.org\u002F10.3390\u002Fmolecules23040965",{"doi":1872},"10.3390\u002Fmolecules23040965",{"id":383,"text":1874,"url":385,"identifiers":1875},"Carlson JR, Bauer BA, Vincent A, Limburg PJ, Wilson T (2007) Reading the tea leaves: anticarcinogenic properties of (-)-epigallocatechin-3-gallate. In: Mayo Clinic Proceedings, vol 6. 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