Molecular Neurobiology

Công bố khoa học tiêu biểu

* Dữ liệu chỉ mang tính chất tham khảo

Sắp xếp:  
Injectable Hydrogel Containing Tauroursodeoxycholic Acid for Anti-neuroinflammatory Therapy After Spinal Cord Injury in Rats
Molecular Neurobiology - - 2020
Gong Ho Han, Seong Jun Kim, Wan‐Kyu Ko, Daye Lee, Jae Seo Lee, Haram Nah, Inbo Han, Seil Sohn
Pinocembrin Suppresses H2O2-Induced Mitochondrial Dysfunction by a Mechanism Dependent on the Nrf2/HO-1 Axis in SH-SY5Y Cells
Molecular Neurobiology - Tập 55 - Trang 989-1003 - 2017
Marcos Roberto de Oliveira, Gustavo da Costa Ferreira, Flávia Bittencourt Brasil, Alessandra Peres
Mitochondria are susceptible to redox impairment, which has been associated with neurodegeneration. These organelles are both a source and target of reactive species. In that context, there is increasing interest in finding natural compounds that modulate mitochondrial function and mitochondria-related signaling in order to prevent or to treat diseases involving mitochondrial impairment. Herein, we investigated whether and how pinocembrin (PB) would prevent mitochondrial dysfunction elicited by the exposure of human neuroblastoma SH-SY5Y cells to hydrogen peroxide (H2O2). PB (25 μM) was administrated for 4 h before H2O2 treatment (300 μM for 24 h). PB prevented H2O2-induced loss of cell viability mitochondrial depolarization in SH-SY5Y cells. PB also attenuated redox impairment in mitochondrial membranes. The production of superoxide anion radical (O2 −•) and nitric oxide (NO•) was alleviated by PB in cells exposed to H2O2. PB suppressed the H2O2-induced inhibition of the tricarboxylic acid (TCA) cycle enzymes aconitase, α-ketoglutarate dehydrogenase, and succinate dehydrogenase. Furthermore, PB induced anti-inflammatory effects by abolishing the H2O2-dependent activation of the nuclear factor-κB (NF-κB) and upregulation of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). The PB-induced antioxidant and anti-inflammatory effects are dependent on the heme oxygenate-1 (HO-1) enzyme and on the activation of the transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2), since HO-1 inhibition (with 0.5 μM ZnPP IX) or Nrf2 silencing (with small interfering RNA (siRNA)) abolished the effects of PB. Overall, PB afforded cytoprotection by the Nrf2/HO-1 axis in H2O2-treated SH-SY5Y cells.
Persistent mitoKATP Activation Is Involved in the Isoflurane-induced Cytotoxicity
Molecular Neurobiology - Tập 54 Số 2 - Trang 1101-1110 - 2017
Yang, Yan, Chen, Xiufang, Min, Haiyan, Song, Shiyu, Zhang, Juan, Fan, Shanshan, Yi, Long, Wang, Hongwei, Gu, Xiaoping, Ma, Zhengliang, Gao, Qian
Isoflurane exposure induces apoptosis in cultured cells and in the developing brain, while the underlying mechanism remains largely unclarified. This study was designed to determine whether the disruption of mitoKATP-mediated ATP balance was involved in the cytotoxicity of isoflurane. Human neuroglioma cells U251 and 7-day-old mice were treated with isoflurane. A specific mitoKATP antagonist 5-HD was used, and the cellular ATP levels, NAD+/NADH ratios, and mitochondrial transmembrane potential (ΔΨm) were measured. Our data showed that the blockage of mitoKATP by 5-HD mitigated the isoflurane-induced ΔΨm disruption, reactive oxygen species (ROS) accumulation, and apoptosis in U251 cells. Moreover, we found that the toxic effect of isoflurane was not observed in the first 2-h exposure; instead, the cellular ATP levels and NAD+/NADH ratios were markedly increased. The reduction of ATP levels and NAD+/NADH ratios was only detected after this initial phase. This dynamical effect of isoflurane was blocked by 5-HD. In contrast, a ROS scavenger NAC sustained the isoflurane-induced ATP elevation. Similar results were observed in animal studies. And again, 5-HD attenuated isoflurane-induced cognitive disorders in the Intellicage test, a system that assesses place learning behavior in a social environment. Our study uncovered a potential mechanism underlying isoflurane’s toxicity with a therapeutic future.
Pro-necrotic Activity of Cationic Mastoparan Peptides in Human Glioblastoma Multiforme Cells Via Membranolytic Action
Molecular Neurobiology - - 2018
Annielle Mendes Brito da Silva, Laíz Costa Silva-Gonçalves, Fernando A. Oliveira, Manoel Arcísio-Miranda
Truyền dẫn synap và tính biến đổi trong hạch hạnh nhân Dịch bởi AI
Molecular Neurobiology - Tập 13 - Trang 1-22 - 1996
Stephen Maren
Nhiều nghiên cứu trên chuột và con người chỉ ra tầm quan trọng của hạch hạnh nhân trong việc tiếp thu và diễn đạt nỗi sợ đã học. Việc xác định hạch hạnh nhân là một cơ sở thần kinh thiết yếu cho điều kiện hóa nỗi sợ đã cho phép thực hiện các nghiên cứu thần kinh sinh lý về các quá trình synap trong hạch hạnh nhân có thể làm trung gian cho điều kiện hóa nỗi sợ. Một cơ chế tế bào có thể cho điều kiện hóa nỗi sợ là sự tăng cường dài hạn (LTP), một sự gia tăng lâu dài trong truyền dẫn synap được gây ra bởi sự kích thích với tần số cao của các nhánh kích thích. Hiện tại, các cơ chế nền tảng cho việc tạo ra và diễn đạt LTP hạch hạnh nhân chỉ mới bắt đầu được hiểu, và có khả năng liên quan đến cả hai loại thụ thể glutamat N-methyl-d-aspartate (NMDA) và α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA). Bài báo này sẽ xem xét các nghiên cứu gần đây về truyền dẫn synap và tính biến đổi trong hạch hạnh nhân nhằm hiểu mối quan hệ của các quá trình này với việc học tập và ghi nhớ những trải nghiệm tiêu cực.
#hạch hạnh nhân #điều kiện hóa nỗi sợ #truyền dẫn synap #tính biến đổi #NMDA #AMPA
AT2R Activation Prevents Microglia Pro-inflammatory Activation in a NOX-Dependent Manner: Inhibition of PKC Activation and p47phox Phosphorylation by PP2A
Molecular Neurobiology - Tập 56 - Trang 3005-3023 - 2018
Shahnawaz Ali Bhat, Anika Sood, Rakesh Shukla, Kashif Hanif
Microglia-induced reactive oxygen species (ROS) production and inflammation play an imperative role in neurodegenerative diseases like Alzheimer’s disease (AD) and Parkinson’s disease (PD). It has been established that angiotensin II type-2 receptor (AT2R) activation is neuroprotective in central nervous system diseases like stroke and AD. However, the involvement of AT2R in NADPH oxidase (NOX)-mediated microglia activation is still elusive. Therefore, the present study investigated the role of AT2R in angiotensin II (Ang II) or Phorbol 12-myristate 13-acetate (PMA)-induced microglia activation in BV2 cells, primary microglia, p47phox knockout (p47KO) microglia, and in vivo. Treatment of microglia with Ang II or PMA induced a significant ROS generation and promoted pro-inflammatory microglia in a NOX-dependent manner. In contrast, AT2R activation by CGP42112A (CGP) inhibited NOX activation, ROS production, and pro-inflammatory microglia activation, while promoting the immunoregulatory microglia. This inhibitory effect of AT2R on NOX and pro-inflammatory activation was attenuated by AT2R antagonist, PD123319. Essentially, NOX inhibition (by DPI) or scavenging cellular ROS (by NAC) or p47KO microglia were immune to Ang II- or PMA-induced pro-inflammatory microglia activation. Mechanistically, AT2R, via activation of protein phosphatase-2A (PP2A), prevented the Ang II- or PMA-induced protein kinase C (PKC) activation and phosphorylation of p47phox, an effect that was reversed by the addition of PP2A inhibitor, Okadaic acid (OA). Importantly, PKC inhibitor, Rottlerin, inhibited the Ang II- or PMA-induced p47phox phosphorylation and ROS generation to the similar extent as AT2R activation. In addition, AT2R activation or p47KO prevented ROS production, pro-inflammatory microglial activation, and sickness behavior in mice model of neuroinflammation. Therefore, the present findings suggested that AT2R, via PP2A-mediated inhibition of PKC, prevents the NOX activation, ROS generation, and subsequent pro-inflammatory activation of microglia.
Arachidonic Acid Induces ARE/Nrf2-Dependent Heme Oxygenase-1 Transcription in Rat Brain Astrocytes
Molecular Neurobiology - - 2018
Chih-Chung Lin, Chien-Chung Yang, Yu‐Wen Chen, Li-Der Hsiao, Chih-Hui Yang
The Fragile X Protein and Genome Function
Molecular Neurobiology - Tập 56 Số 1 - Trang 711-721 - 2019
Thomas C. Dockendorff, Mariano Labrador
Correction to: lncRNA NONRATT021972 siRNA Decreases Diabetic Neuropathic Pain Mediated by the P2X3 Receptor in Dorsal Root Ganglia
Molecular Neurobiology - Tập 56 - Trang 6656-6657 - 2019
Haiying Peng, Lifang Zou, Jinyan Xie, Hong Wu, Bing Wu, Gaochun Zhu, Qiulan Lv, Xi Zhang, Shuangmei Liu, Guilin Li, Hong Xu, Yun Gao, Changshui Xu, Chunping Zhang, Shouyu Wang, Yun Xue, Shangdong Liang
In the original version of this article “lncRNA NONRATT021972 siRNA Decreases Diabetic Neuropathic Pain Mediated by the P2X3 Receptor in Dorsal Root Ganglia”, which we have published in Mol Neurobiol (2017) 54:511–523.
The Diagnostic Value of Whole-Exome Sequencing in a Spectrum of Rare Neurological Disorders Associated with Cerebellar Atrophy
Molecular Neurobiology - - Trang 1-13 - 2023
Engy A. Ashaat, Hoda A. Ahmed, Nesma M. Elaraby, Alaaeldin Fayez, Ammal M. Metwally, Mona K. Mekkawy, Dalia Farouk Hussen, Neveen A. Ashaat, Rasha M. Elhossini, Heba Ahmed ElAwady, Randa H. A. Abdelgawad, Mona El Gammal, Mohamed Ahmed Al Kersh, Dina Amin Saleh
Several neurological disorders, neurodevelopmental disorders, and neurodegenerative disorders have a genetic element with various clinical presentations ranging from mild to severe presentation. Neurological disorders are rare multifactorial disorders characterized by dysfunction and degeneration of synapses, neurons, and glial cells which are essential for movement, coordination, muscle strength, sensation, and cognition. The cerebellum might be involved at any time, either during development and maturation or later in life. Herein, we describe a spectrum of NDDs and NDs in seven patients from six Egyptian families. The core clinical and radiological features of our patients included dysmorphic features, neurodevelopmental delay or regression, gait abnormalities, skeletal deformities, visual impairment, seizures, and cerebellar atrophy. Previously unreported clinical phenotypic findings were recorded. Whole-exome sequencing (WES) was performed followed by an in silico analysis of the detected genetic variants’ effect on the protein structure. Three novel variants were identified in three genes MFSD8, AGTPBP1, and APTX, and other previously reported three variants have been detected in “TPP1, AGTPBP1, and PCDHGC4” genes. In this cohort, we described the detailed unique phenotypic characteristics given the identified genetic profile in patients with neurological “neurodevelopmental disorders and neurodegenerative disorders” disorders associated with cerebellar atrophy, hence expanding the mutational spectrum of such disorders.
Tổng số: 4,547   
  • 1
  • 2
  • 3
  • 4
  • 5
  • 6
  • 10