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[3H] gelatin degradation by glomeruli was markedly inhibited by EDTA (10 mM: -89 +\u002F- 2.3%) and o-phenanthroline (2 mM: -72 +\u002F- 0.1%), inhibitors of metalloproteinases. No significant inhibition of [3H]gelatin degradation was observed with inhibitors of serine or cysteine proteinases. Most (greater than 80%) of the glomerular metalloproteinase (GLOMP) activity was associated with the pellet after centrifugation of sonicated glomeruli at 100,000 g for 90 min. The pH optimum for gelatin degradation by sonicated glomeruli was approximately pH 8.5. Sodium dodecyl sulfate substrate (gelatin)-polyacrylamide gel electrophoresis revealed a single major band of EDTA-inhibitable gelatin-degrading activity with a molecular mass of approximately 116-125 kDa. The GLOMP activity was not inhibited by tissue inhibitors of metalloproteinases, did not appear to be latent, and was not activated by organomercurial activators of several latent metalloproteinases. GLOMP activity was increased 3.4-fold after incubation with trypsin (20 micrograms\u002Fml, 25 min, 22 degrees C). These data indicate that GLOMP is distinct from the previously described matrix metalloproteinases, as well as other metalloproteinases present in the kidney, including the gelatinase secreted by cultured mesangial cells, Meprin, and endopeptidase 24.11 (enkephalinase, EC 3.4.24.11). \u003C\u002Fjats:p>",{"EN":155},"A novel metalloproteinase present in freshly isolated rat glomeruli",{"VOID":157},"1901457",{"VOID":159},"10.1152\u002Fajprenal.1991.260.4.f555","PUBLICATION","VERIFIED","Auto Verify",[164],"EN","https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.1991.260.4.F555",[167,186,203,220,235],{"id":168,"sortIndex":25,"researcher":24,"roles":169,"affiliations":170,"properties":179,"displayName":183,"givenName":24,"familyName":24},"fd3431c8-e997-442b-a677-305e6291ce06",[],[171],{"id":172,"sortIndex":25,"affiliation":173,"properties":24},"fab85361-994c-4c74-8f9b-0fa0f8a2723d",{"id":172,"createTime":24,"updateTime":24,"relativeEntities":174,"slug":24,"properties":175,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":178,"statistic":24},[],{"title":176},{"VI":177},"Department of Biochemistry, Tulane Medical School, New Orleans, Louisiana 70112",[],{"orcid":180,"title":182,"openalex":184},{"VOID":181},"https:\u002F\u002Forcid.org\u002F0009-0007-3073-7520",{"EN":183},"Quoc‐Tuan Le",{"VOID":185},"A5057144965",{"id":187,"sortIndex":101,"researcher":24,"roles":188,"affiliations":189,"properties":196,"displayName":200,"givenName":24,"familyName":24},"29cc1299-5344-4b2c-bfce-90e2848ec872",[],[190],{"id":172,"sortIndex":25,"affiliation":191,"properties":24},{"id":172,"createTime":24,"updateTime":24,"relativeEntities":192,"slug":24,"properties":193,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":195,"statistic":24},[],{"title":194},{"VI":177},[],{"orcid":197,"title":199,"openalex":201},{"VOID":198},"https:\u002F\u002Forcid.org\u002F0009-0006-2403-8136",{"EN":200},"Sudhir V. 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Although exercise programs have demonstrated a positive effect on physiological outcomes such as cardiovascular function and strength, there is a reduced focus on physical function. The aim of this review was to determine whether exercise programs improve objective measures of physical function indicative of activities of daily living for patients with end-stage kidney disease on dialysis. A systematic search of Medline, Embase, the Cochrane Central Register of Controlled Trials, and Cumulative Index to Nursing and Allied Health Literature identified 27 randomized control trials. Only randomized control trials using an exercise intervention or significant muscular activation in the intervention, a usual care, nonexercising control group, and at least one objective measure of physical function were included. Participants were ≥18 yr of age, with end-stage kidney disease, undergoing hemo- or peritoneal dialysis. Systematic review of the literature and quality assessment of the included studies used the Cochrane Collaboration’s tool for assessing risk bias. A meta-analysis was completed for the 6-min walk test. Data from 27 studies with 1,156 participants showed that exercise, regardless of modality, generally increased 6-min walk test distance, sit-to-stand time or repetitions, and grip strength as well as step and stair climb times or repetitions, dynamic mobility, and short physical performance battery scores. From the evidence available, exercise, regardless of modality, improved objective measures of physical function for end-stage kidney disease patients undergoing dialysis. 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chuyển canxi, ống thận xa, hormone tuyến cận giáp, amiloride, thụ động",{"VOID":763},"W2417036006",{"EN":765,"VI":766},"\u003Cjats:p> The mechanism of Ca2+ transport by various segments of the distal nephron was studied in vitro using the isolated perfused tubule technique. Calcium absorption in the distal convoluted tubule (DCT) and the granular portion of the cortical collecting duct (CCTg) was significantly enhanced in the presence of parathyroid hormone (PTH), 3 X 10(-2) U\u002Fml. Na+ was absorbed from and K+ was secreted into the lumen of the DCT. The presence of amiloride (5 X 10(-5) M) or furosemide (5 X 10(-5) M) in the perfusate of DCT each caused a partial inhibition of Na+ but not Ca2+ absorption. The foregoing result with Na+ is consistent with the heterogeneous nature of DCT. Net Na+ absorption and K+ secretion also occurred in the CCTg; both processes were completely inhibited by amiloride. Ca2+ absorption occurred in the thick ascending limb of Henle's loop; it was not enhanced by PTH, and the results were consistent with passive movement. No net Ca2+ movement was observed in the nongranular (light) segment of the cortical collecting tubule in the presence or absence of PTH or dibutyryl cyclic adenosine monophosphate. \u003C\u002Fjats:p>","\u003Cjats:p> Cơ chế vận chuyển Ca2+ bởi các đoạn khác nhau của ống thận xa đã được nghiên cứu in vitro bằng kỹ thuật ống dẫn máu cách ly. Sự hấp thu canxi trong ống thận xoắn xa (DCT) và phần hạt của ống thu thập vỏ (CCTg) đã được tăng cường một cách đáng kể trong sự hiện diện của hormone tuyến cận giáp (PTH), 3 X 10(-2) U\u002Fml. Na+ được hấp thu từ và K+ được bài tiết vào lòng DCT. Sự hiện diện của amiloride (5 X 10(-5) M) hoặc furosemide (5 X 10(-5) M) trong dung dịch perfusate của DCT đã làm giảm một phần sự hấp thu Na+ nhưng không ảnh hưởng đến sự hấp thu Ca2+. Kết quả trên với Na+ phù hợp với tính chất không đồng nhất của DCT. Sự hấp thu Na+ ròng và bài tiết K+ cũng xảy ra trong CCTg; cả hai quá trình này đều bị ức chế hoàn toàn bởi amiloride. Sự hấp thu Ca2+ diễn ra trong nhánh mỏng hướng lên của vòng Henle; quá trình này không được tăng cường bởi PTH và kết quả phù hợp với sự vận chuyển thụ động. Không có sự dịch chuyển Ca2+ ròng nào được quan sát thấy trong đoạn không hạt (nhẹ) của ống thu thập vỏ, bất kể có mặt hay không có PTH hoặc dibutyryl cyclic adenosine monophosphate.",{"EN":768,"VI":769},"Calcium transport across segments of the rabbit distal nephron in vitro","Sự vận chuyển canxi qua các đoạn của ống thận xa của thỏ trong môi trường in vitro",{"VOID":771},"211862",{"VOID":773},"10.1152\u002Fajprenal.1978.235.4.f367","2024-09-02T18:44:15.453+00:00","Author affiliation is blank",[164],[778],"VI","https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.1978.235.4.F367",[781,790],{"id":782,"sortIndex":25,"researcher":24,"roles":783,"affiliations":784,"properties":785,"displayName":787,"givenName":24,"familyName":24},"27e08adf-678b-4392-8d46-5a72eca837ac",[],[],{"title":786,"openalex":788},{"EN":787},"G. R. 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Because proteinuria is a hallmark for kidney disease, we examined the relationship between proteinuria and tubular induction of HO-1, specifically questioning whether increased trafficking of protein across the renal tubular epithelium, as a consequence of proteinuria, induces tubular expression of HO-1. We examined a model of glomerular proteinuria induced by daily injections of BSA, which is associated with increased tubular uptake of filtered protein, and a model of tubular proteinuria induced by maleate, the latter exhibiting decreased tubular uptake and trafficking of protein. The BSA model of glomerular proteinuria failed to exhibit induction of HO-1; HO-1 was not induced in proximal tubular epithelial cells exposed to BSA. In contrast, in maleate nephropathy wherein tubular uptake of protein is decreased because of generalized proximal tubular injury induced by maleate, HO-1 was strongly induced in proximal tubules; inhibition of HO activity in maleate nephropathy worsened proteinuria, renal histological injury, and apoptosis. In renal proximal tubular epithelial cells, maleate induced HO-1 and caused apoptosis, the latter increased when HO activity was inhibited. From these studies, we conclude that expression of HO-1 in the diseased kidney cannot be ascribed to the tubular uptake and metabolism of protein such as albumin, and that the expression of HO-1 in a model of tubular proteinuria reflects a functionally significant stress response to toxin-induced proximal tubular injury.\u003C\u002Fjats:p>","\u003Cjats:p>Heme oxygenase-1 (HO-1), một gen bảo vệ tế bào, thường được kích thích trong các ống thận ở thận bị bệnh. Do proteinuria là dấu hiệu đặc trưng của bệnh thận, chúng tôi đã xem xét mối quan hệ giữa proteinuria và việc kích thích HO-1 trong ống thận, cụ thể là đặt câu hỏi liệu việc gia tăng lưu thông protein qua biểu mô ống thận, do kết quả của proteinuria, có kích thích biểu hiện HO-1 trong ống thận hay không. Chúng tôi đã nghiên cứu một mô hình proteinuria cầu thận do tiêm BSA hàng ngày, mô hình này có liên quan đến việc tăng cường hấp thụ protein từ ống thận và một mô hình proteinuria ống thận do maleate, mô hình sau cho thấy giảm hấp thụ và lưu thông protein ở ống thận. Mô hình proteinuria cầu thận với BSA không cho thấy sự kích thích của HO-1; HO-1 không được kích thích trong các tế bào biểu mô ống thận gần gũi tiếp xúc với BSA. Ngược lại, trong bệnh thận maleate mà trong đó việc hấp thụ protein ở ống thận bị giảm do tổn thương ống thận gần gũi toàn diện do maleate gây ra, HO-1 đã được kích thích mạnh mẽ ở ống thận gần gũi; việc ức chế hoạt động của HO trong bệnh thận maleate làm tình trạng proteinuria trở nên xấu đi, tổn thương mô thận, và apoptosis cũng tăng lên. Trong các tế bào biểu mô ống thận gần gũi, maleate kích thích HO-1 và gây ra apoptosis, trong đó tăng cường hơn khi hoạt động của HO bị ức chế. Từ những nghiên cứu này, chúng tôi kết luận rằng biểu hiện của HO-1 trong thận bị bệnh không thể được quy cho hấp thụ và chuyển hóa protein như albumin trong ống thận, và rằng biểu hiện của HO-1 trong mô hình proteinuria ống thận phản ánh một phản ứng căng thẳng có ý nghĩa chức năng đối với tổn thương ống thận do độc tố gây ra.\u003C\u002Fjats:p>",{"EN":876,"VI":877},"Proteinuria as a determinant of renal expression of heme oxygenase-1: studies in models of glomerular and tubular proteinuria in the rat","Proteinuria như một yếu tố quyết định sự biểu hiện của heme oxygenase-1 ở thận: nghiên cứu trong các mô hình proteinuria cầu thận và ống thận ở chuột",{"VOID":879},"16118392",{"VOID":881},"10.1152\u002Fajprenal.00230.2005","2025-01-28T13:19:11.688+00:00",[164],[778],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00230.2005",[887,906,925,940,957,968],{"id":888,"sortIndex":25,"researcher":24,"roles":889,"affiliations":890,"properties":899,"displayName":903,"givenName":24,"familyName":24},"b0876c29-1388-4a4d-98fe-0f901d10afe6",[],[891],{"id":892,"sortIndex":25,"affiliation":893,"properties":24},"2f7de2dc-3544-4c13-8fdf-f68051d76f21",{"id":892,"createTime":24,"updateTime":24,"relativeEntities":894,"slug":24,"properties":895,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":898,"statistic":24},[],{"title":896},{"EN":897},"Division of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, 55905, USA",[],{"orcid":900,"title":902,"openalex":904},{"VOID":901},"https:\u002F\u002Forcid.org\u002F0000-0001-6628-4411",{"EN":903},"José Pedraza-Chaverrı́",{"VOID":905},"A5026722432",{"id":907,"sortIndex":101,"researcher":24,"roles":908,"affiliations":909,"properties":918,"displayName":922,"givenName":24,"familyName":24},"bdc51127-0c49-4dd3-a5f4-39e41203e977",[],[910],{"id":911,"sortIndex":25,"affiliation":912,"properties":24},"97803957-cdc4-4945-bd32-dbb28b17b32d",{"id":911,"createTime":24,"updateTime":24,"relativeEntities":913,"slug":24,"properties":914,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":917,"statistic":24},[],{"title":915},{"EN":916},"Mayo Clinic Rochester-MN",[],{"orcid":919,"title":921,"openalex":923},{"VOID":920},"https:\u002F\u002Forcid.org\u002F0000-0002-0099-5330",{"EN":922},"Narayana S. 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We hypothesized that CO would protect ischemia-reperfusion (I\u002FR) injury of transplanted organs, and the efficacy of CO was studied in the rat kidney transplantation model. A Lewis rat kidney graft, preserved in University of Wisconsin solution at 4°C for 24 h, was orthotopically transplanted into syngeneic rats. Recipients were maintained in room air or exposed to CO (250 ppm) in air for 1 h before and 24 h after transplantation. Animals were killed 1, 3, 6, and 24 h after transplantation to assess efficacy of inhaled CO. Rapid upregulation of mRNA for IL-6, IL-1β, TNF-α, ICAM-1, heme oxygenase-1, and inducible nitric oxide synthase was observed within 3 h after transplantation in the control grafts of air-exposed recipients, associating with histopathological evidences of acute tubular necrosis, interstitial hemorrhage, and edema. In contrast, the increase of inflammatory mediators was markedly inhibited in kidney grafts of CO-treated recipients, which correlated with improved renal cortical blood flow. Further detailed morphological analyses revealed that CO preserved the glomerular vascular architecture and podocyte viability with less apoptosis of tubular epithelial cells and less ED1\u003Cjats:sup>+\u003C\u002Fjats:sup>macrophage infiltration. CO inhalation resulted in improved serum creatinine levels and clearance, and animal survival was significantly improved with CO to 60.5 from 25 days in untreated controls. The study demonstrates that exposure of kidney graft recipients to CO at a low concentration can impart significant protective effects against renal I\u002FR injury and improve function of renal grafts.\u003C\u002Fjats:p>","\u003Cjats:p>Carbon monoxide (CO), một sản phẩm của quá trình chuyển hóa heme do các enzyme heme oxygenases, được biết đến với khả năng bảo vệ chống lại stress oxy hóa. Chúng tôi giả thuyết rằng CO sẽ bảo vệ tổn thương thiếu máu - tái tưới máu (I\u002FR) của các cơ quan được ghép, và hiệu quả của CO đã được nghiên cứu trong mô hình ghép thận chuột cống. Một mảnh thận chuột cống Lewis, được bảo quản trong dung dịch University of Wisconsin ở 4°C trong 24 giờ, đã được ghép vào vị trí tự nhiên trong các chuột đồng huyết. Những con chuột nhận ghép được duy trì trong không khí phòng hoặc tiếp xúc với CO (250 ppm) trong không khí trong 1 giờ trước và 24 giờ sau khi ghép. Động vật đã bị giết 1, 3, 6, và 24 giờ sau khi ghép để đánh giá hiệu quả của CO hít vào. Sự gia tăng nhanh chóng của mRNA cho IL-6, IL-1β, TNF-α, ICAM-1, heme oxygenase-1, và synthase nitric oxide cảm ứng đã được quan sát thấy trong vòng 3 giờ sau khi ghép ở các mảnh ghép kiểm soát của những con chuột được tiếp xúc với không khí, liên quan đến các bằng chứng mô học của hoại tử ống cấp tính, chảy máu mô kẽ, và phù nề. Ngược lại, sự gia tăng của các chất trung gian viêm đã bị ức chế rõ rệt ở các mảnh ghép thận của những con chuột được điều trị bằng CO, điều này tương quan với việc cải thiện lưu lượng máu vỏ thận. Các phân tích hình thái học chi tiết hơn cho thấy rằng CO duy trì cấu trúc mạch máu cầu thận và sự sống sót của tế bào podocyte với ít sự apoptosis của các tế bào biểu mô ống thận và ít sự xâm nhập của tế bào đại thực bào ED1\u003Cjats:sup>+\u003C\u002Fjats:sup>. Việc hít CO đã dẫn đến cải thiện mức creatinine huyết thanh và độ thanh thải, và sự sống sót của động vật đã được cải thiện đáng kể với CO từ 25 ngày lên 60,5 ngày ở các trường hợp đối chứng không điều trị. Nghiên cứu chứng minh rằng việc tiếp xúc với CO ở nồng độ thấp ở những người nhận ghép thận có thể mang lại hiệu ứng bảo vệ đáng kể chống lại tổn thương I\u002FR thận và cải thiện chức năng của các mảnh ghép thận.\u003C\u002Fjats:p>",{"EN":1196,"VI":1197},"Protection of transplant-induced renal ischemia-reperfusion injury with carbon monoxide","Bảo vệ tổn thương thiếu máu - tái tưới máu ở thận ghép do carbon monoxide",{"VOID":1199},"15292046",{"VOID":1201},"10.1152\u002Fajprenal.00158.2004","2025-01-28T13:19:14.044+00:00",[164],[778],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00158.2004",[1207,1226,1243,1258,1273,1290,1307,1322,1339],{"id":1208,"sortIndex":25,"researcher":24,"roles":1209,"affiliations":1210,"properties":1219,"displayName":1223,"givenName":24,"familyName":24},"e0039837-2cbb-4c98-911a-2ba77e551751",[],[1211],{"id":1212,"sortIndex":25,"affiliation":1213,"properties":24},"11f150e1-39bb-4523-8e2a-abdd674e2a66",{"id":1212,"createTime":24,"updateTime":24,"relativeEntities":1214,"slug":24,"properties":1215,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1218,"statistic":24},[],{"title":1216},{"EN":1217},"University of Pittsburgh, Pittsburgh, United States",[],{"orcid":1220,"title":1222,"openalex":1224},{"VOID":1221},"https:\u002F\u002Forcid.org\u002F0000-0003-2267-5386",{"EN":1223},"João Seda Neto",{"VOID":1225},"A5061616341",{"id":1227,"sortIndex":101,"researcher":24,"roles":1228,"affiliations":1229,"properties":1236,"displayName":1240,"givenName":24,"familyName":24},"51f1245f-db00-4511-8a22-7e0f3646c317",[],[1230],{"id":1212,"sortIndex":25,"affiliation":1231,"properties":24},{"id":1212,"createTime":24,"updateTime":24,"relativeEntities":1232,"slug":24,"properties":1233,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1235,"statistic":24},[],{"title":1234},{"EN":1217},[],{"orcid":1237,"title":1239,"openalex":1241},{"VOID":1238},"https:\u002F\u002Forcid.org\u002F0000-0002-6818-2985",{"EN":1240},"Atsunori Nakao",{"VOID":1242},"A5064168914",{"id":1244,"sortIndex":104,"researcher":24,"roles":1245,"affiliations":1246,"properties":1253,"displayName":1255,"givenName":24,"familyName":24},"2c402e5f-4354-438c-9fd0-98577637084b",[],[1247],{"id":1212,"sortIndex":25,"affiliation":1248,"properties":24},{"id":1212,"createTime":24,"updateTime":24,"relativeEntities":1249,"slug":24,"properties":1250,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1252,"statistic":24},[],{"title":1251},{"EN":1217},[],{"title":1254,"openalex":1256},{"EN":1255},"Kei Kimizuka",{"VOID":1257},"A5065387301",{"id":1259,"sortIndex":105,"researcher":24,"roles":1260,"affiliations":1261,"properties":1268,"displayName":1270,"givenName":24,"familyName":24},"8449ff63-3c30-411c-909a-d72d756ec3ea",[],[1262],{"id":1212,"sortIndex":25,"affiliation":1263,"properties":24},{"id":1212,"createTime":24,"updateTime":24,"relativeEntities":1264,"slug":24,"properties":1265,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1267,"statistic":24},[],{"title":1266},{"EN":1217},[],{"title":1269,"openalex":1271},{"EN":1270},"Anna Jeanine Romanosky",{"VOID":1272},"A5044939421",{"id":1274,"sortIndex":237,"researcher":24,"roles":1275,"affiliations":1276,"properties":1283,"displayName":1287,"givenName":24,"familyName":24},"0dbf84c8-fd34-461c-b8c9-2cbef49f0bc6",[],[1277],{"id":1212,"sortIndex":25,"affiliation":1278,"properties":24},{"id":1212,"createTime":24,"updateTime":24,"relativeEntities":1279,"slug":24,"properties":1280,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1282,"statistic":24},[],{"title":1281},{"EN":1217},[],{"orcid":1284,"title":1286,"openalex":1288},{"VOID":1285},"https:\u002F\u002Forcid.org\u002F0000-0002-1833-7010",{"EN":1287},"Donna B. 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Possible role of angiotensin II.Am J Pathol114: 157–163, 1984.",{},{"id":24,"text":1520,"url":24,"identifiers":1521},"10.1038\u002Fsj.bjp.0702212",{"doi":1520},{"id":24,"text":1523,"url":24,"identifiers":1524},"10.1016\u002FS0022-5347(17)36036-6",{"doi":1523},{"id":24,"text":1526,"url":24,"identifiers":1527},"Savill J.Apoptosis and the kidney.J Am Soc Nephrol5: 12–21, 1994.",{"doi":1528},"10.1681\u002FASN.V5112",{"id":24,"text":1530,"url":24,"identifiers":1531},"10.1081\u002FJDI-100101955",{"doi":1530},{"id":24,"text":1533,"url":24,"identifiers":1534},"10.1097\u002F00041552-200007000-00015",{"doi":1533},{"id":24,"text":1536,"url":24,"identifiers":1537},"10.1016\u002FS0022-5347(01)66023-3",{"doi":1536},{"id":24,"text":1539,"url":24,"identifiers":1540},"10.1093\u002Femboj\u002Fcdf516",{"doi":1539},{"id":24,"text":1542,"url":24,"identifiers":1543},"10.1172\u002FJCI119457",{"doi":1542},{"id":24,"text":1545,"url":24,"identifiers":1546},"10.1126\u002Fscience.281.5381.1312",{"doi":1545},{"id":24,"text":1548,"url":24,"identifiers":1549},"10.1152\u002Fajprenal.1999.277.6.F882",{"doi":1548},{"id":24,"text":1551,"url":24,"identifiers":1552},"10.1016\u002F0006-2952(91)90658-R",{"doi":1551},{"id":24,"text":1554,"url":24,"identifiers":1555},"10.1002\u002F(SICI)1099-1263(199909\u002F10)19:5\u003C379::AID-JAT563>3.0.CO;2-8",{"doi":1554},{"id":24,"text":1557,"url":24,"identifiers":1558},"10.1038\u002Fki.1986.270",{"doi":1557},{"id":24,"text":1560,"url":24,"identifiers":1561},"10.1038\u002Fki.1984.45",{"doi":1560},{"id":24,"text":1563,"url":24,"identifiers":1564},"10.1136\u002Fthorax.57.9.779",{"doi":1563},{"id":24,"text":1566,"url":24,"identifiers":1567},"Zager RA, Fuerstenberg SM, Baehr PH, Myerson D, and Torok-Storb B.An evaluation of antioxidant effects on recovery from postischemic acute renal failure.J Am Soc Nephrol4: 1588–1597, 1994.",{"doi":1568},"10.1681\u002FASN.V481588",{"id":24,"text":1570,"url":24,"identifiers":1571},"10.1074\u002Fjbc.M208419200",{"doi":1570},{"id":24,"text":1573,"url":24,"identifiers":1574},"10.1016\u002FS0022-3468(97)90388-2",{"doi":1573},{"id":1576,"createTime":1577,"updateTime":1578,"relativeEntities":1579,"slug":1580,"properties":1581,"entityType":160,"verifyStatus":161,"verifyTime":1577,"verifyNote":162,"languages":1597,"translateLanguages":1598,"viewCount":25,"primaryUrl":1599,"fullTextUrl":24,"authors":1600,"publicationType":251,"publisherRelationship":1669,"citationCount":1724,"citationInfo":1725,"publishDate":1728,"publishYear":1726,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":1729,"openAccess":24,"references":1730,"isForceReanalyzing":316},"db459d89-48ec-41ca-83b7-83f3107a1693","2025-01-28T13:19:23.291+00:00","2025-02-12T16:17:43.535+00:00",[],"Nitric-oxide-synthesis-influences-the-renal-vascular-response-to-heme-oxygenase-inhibition",{"mag":1582,"keywords":1584,"openalex":1585,"abstract":1587,"title":1590,"pm":1593,"doi":1595},{"VOID":1583},"2127239181",{"VI":869},{"VOID":1586},"W2127239181",{"EN":1588,"VI":1589},"\u003Cjats:p> We studied the effects of the heme oxygenase (HO) inhibitor stannous mesoporphyrin (SnMP; 40 μmol\u002Fkg iv) on renal hemodynamics in anesthetized rats with and without 48-h pretreatment with N \u003Cjats:sup>G\u003C\u002Fjats:sup>-nitro-l-arginine methyl ester (l-NAME), an inhibitor of nitric oxide (NO) synthesis. SnMP decreased renal blood flow (RBF) and increased renal vascular resistance (RVR) in both groups. The SnMP-induced reduction of RBF inl-NAME-pretreated rats was more prominent than in rats without pretreatment (43 ± 7 vs. 13 ± 3%) as was the SnMP-induced elevation of RVR (87 ± 31 vs. 14 ± 5%). The renal vasoconstrictor effect of SnMP is linked, in part, to amplification of prevailing neurohormonal constrictor mechanisms, since in l-NAME-pretreated rats it was prevented by concurrent administration of prazosin or losartan. However, SnMP (15 μmol\u002Fl) also elicits vasoconstriction in isolated, pressurized renal interlobular arteries and the response is more intense in vessels obtained from l-NAME-pretreated rats than from rats without pretreatment. These data indicate that the status of NO synthesis conditions the vascular response to HO inhibition in the rat kidney. \u003C\u002Fjats:p>","\u003Cjats:p> Chúng tôi đã nghiên cứu tác động của chất ức chế heme oxygenase (HO) là stannous mesoporphyrin (SnMP; 40 μmol\u002Fkg iv) đối với huyết động học thận ở chuột gây mê với và không có điều trị trước 48 giờ bằng N \u003Cjats:sup>G\u003C\u002Fjats:sup>-nitro-l-arginine methyl ester (l-NAME), một chất ức chế tổng hợp nitric oxide (NO). SnMP làm giảm lưu lượng máu thận (RBF) và tăng kháng lực mạch máu thận (RVR) ở cả hai nhóm. Sự giảm RBF do SnMP gây ra ở chuột đã được điều trị bằng l-NAME rõ rệt hơn so với chuột không điều trị trước (43 ± 7 so với 13 ± 3%) như cũng tương tự đối với sự gia tăng RVR do SnMP gây ra (87 ± 31 so với 14 ± 5%). Hiệu ứng co mạch thận của SnMP liên quan phần nào đến việc khuếch đại các cơ chế co mạch thần kinh-hormone hiện có, bởi vì ở chuột đã được điều trị bằng l-NAME, hiệu ứng này bị ngăn chặn bởi việc sử dụng đồng thời prazosin hoặc losartan. Tuy nhiên, SnMP (15 μmol\u002Fl) cũng gây ra co mạch trong các động mạch liên thận tách rời, có áp lực, và phản ứng này mạnh mẽ hơn trong các mạch được lấy từ chuột đã được điều trị bằng l-NAME so với chuột không có điều trị trước. Những dữ liệu này chỉ ra rằng trạng thái tổng hợp NO ảnh hưởng đến phản ứng mạch máu đối với việc ức chế HO trong thận chuột.\u003C\u002Fjats:p>",{"EN":1591,"VI":1592},"Nitric oxide synthesis influences the renal vascular  response to heme oxygenase inhibition","Tổng hợp nitric oxide ảnh hưởng đến phản ứng mạch máu thận khi ức chế heme 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We previously demonstrated that carbon monoxide (CO) stimulates the apical 70-pS K\u003Cjats:sup>+\u003C\u002Fjats:sup> channel in the thick ascending limb (TAL) of the rat kidney (Liu HJ, Mount DB, Nasjletti A, and Wang WH. J Clin Invest 103: 963-970, 1999). Because the apical K\u003Cjats:sup>+\u003C\u002Fjats:sup> channel plays a key role in K\u003Cjats:sup>+\u003C\u002Fjats:sup> recycling, we tested the hypothesis that heme oxygenase (HO)-dependent metabolites of heme may affect Na\u003Cjats:sup>+\u003C\u002Fjats:sup> transport in the TAL. We used in vivo microperfusion to study the effect of chromium mesoporphyrin (CrMP), an inhibitor of HO, on fluid absorption ( J\u003Cjats:sub>v\u003C\u002Fjats:sub>) and Na\u003Cjats:sup>+\u003C\u002Fjats:sup> absorption ( J\u003Cjats:sub>Na\u003C\u002Fjats:sub>) in the loop of Henle and renal clearance methods to examine the effect of CrMP on renal sodium excretion. Microperfusion experiments demonstrated that addition of CrMP to the loop of Henle decreased J\u003Cjats:sub>v\u003C\u002Fjats:sub> by 13% and J\u003Cjats:sub>Na\u003C\u002Fjats:sub> by 20% in animals on normal rat chow and caused a decrease in J\u003Cjats:sub>v\u003C\u002Fjats:sub> (39%) and J\u003Cjats:sub>Na\u003C\u002Fjats:sub> (40%) in rats on a high-K\u003Cjats:sup>+\u003C\u002Fjats:sup> (HK) diet. The effect of CrMP is the result of inhibition of HO because addition of MgPP, an analog of CrMP that does not inhibit HO, had no effect on J\u003Cjats:sub>v\u003C\u002Fjats:sub>. Western blot analysis showed that HO-2 is expressed in the kidney and that the level of HO-2 was significantly elevated in animals on a HK diet. Renal clearance studies demonstrated that the infusion of CrMP increased the excretion of urinary Na\u003Cjats:sup>+\u003C\u002Fjats:sup> (E\u003Cjats:sub>Na\u003C\u002Fjats:sub>) and volume (UV) without changes in glomerular filtration rate. The effect of CrMP on E\u003Cjats:sub>Na\u003C\u002Fjats:sub> and UV was larger in HK rats than those kept on normal chow. We conclude that HK intake increases HO-2 expression in the kidney and that HO-dependent metabolites of heme, presumably CO, play a significant role in the regulation of Na\u003Cjats:sup>+\u003C\u002Fjats:sup> transport in the loop of Henle. \u003C\u002Fjats:p>","\u003Cjats:p> Chúng tôi đã chứng minh trước đây rằng monoxit cacbon (CO) kích thích kênh K\u003Cjats:sup>+\u003C\u002Fjats:sup> 70-pS trên bề mặt apical của nhánh dày (TAL) trong thận chuột (Liu HJ, Mount DB, Nasjletti A, và Wang WH. J Clin Invest 103: 963-970, 1999). Bởi vì kênh K\u003Cjats:sup>+\u003C\u002Fjats:sup> ở bề mặt apical đóng vai trò quan trọng trong việc tái hấp thu K\u003Cjats:sup>+\u003C\u002Fjats:sup>, chúng tôi đã thử nghiệm giả thuyết rằng các chuyển hóa phẩm phụ của heme phụ thuộc vào heme oxygenase (HO) có thể ảnh hưởng đến sự vận chuyển Na\u003Cjats:sup>+\u003C\u002Fjats:sup> trong TAL. Chúng tôi đã sử dụng vi phẫu in vivo để nghiên cứu ảnh hưởng của chromium mesoporphyrin (CrMP), một tác nhân ức chế HO, đến sự hấp thu dịch (J\u003Cjats:sub>v\u003C\u002Fjats:sub>) và hấp thu Na\u003Cjats:sup>+\u003C\u002Fjats:sup> (J\u003Cjats:sub>Na\u003C\u002Fjats:sub>) trong ống Henle và các phương pháp thanh thải thận để xem xét tác động của CrMP đến sự bài tiết natri trong thận. Các thí nghiệm vi phẫu đã chứng minh rằng việc thêm CrMP vào ống Henle làm giảm J\u003Cjats:sub>v\u003C\u002Fjats:sub> 13% và J\u003Cjats:sub>Na\u003C\u002Fjats:sub> 20% ở động vật ăn thức ăn bình thường, và gây ra sự giảm J\u003Cjats:sub>v\u003C\u002Fjats:sub> (39%) và J\u003Cjats:sub>Na\u003C\u002Fjats:sub> (40%) ở chuột ăn chế độ ăn giàu K\u003Cjats:sup>+\u003C\u002Fjats:sup> (HK). Tác động của CrMP là kết quả của sự ức chế HO vì việc thêm MgPP, một đồng phân của CrMP mà không ức chế HO, không có tác động đến J\u003Cjats:sub>v\u003C\u002Fjats:sub>. Phân tích Western blot cho thấy HO-2 được biểu hiện trong thận và mức độ của HO-2 đã tăng đáng kể ở động vật ăn chế độ ăn HK. Các nghiên cứu thanh thải thận chứng minh rằng việc truyền CrMP làm tăng bài tiết Na\u003Cjats:sup>+\u003C\u002Fjats:sup> trong nước tiểu (E\u003Cjats:sub>Na\u003C\u002Fjats:sub>) và thể tích (UV) mà không có sự thay đổi trong tỷ lệ lọc cầu thận. Tác động của CrMP lên E\u003Cjats:sub>Na\u003C\u002Fjats:sub> và UV lớn hơn ở chuột HK so với những con ăn chế độ ăn bình thường. Chúng tôi kết luận rằng việc tiêu thụ HK làm tăng sự biểu hiện của HO-2 trong thận và các chuyển hóa phẩm phụ của heme phụ thuộc vào HO, có thể là CO, đóng vai trò quan trọng trong việc điều hòa vận chuyển Na\u003Cjats:sup>+\u003C\u002Fjats:sup> trong ống Henle.\u003C\u002Fjats:p>",{"EN":1827,"VI":1828},"Inhibition of heme oxygenase decreases sodium and fluid absorption in the  loop of Henle","Sự ức chế heme oxygenase làm giảm hấp thu natri và dịch ở ống Henle",{"VOID":1830},"12890663",{"VOID":1832},"10.1152\u002Fajprenal.00135.2003",[164],[778],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00135.2003",[1837,1856,1865,1874,1883,1902,1911],{"id":1838,"sortIndex":25,"researcher":24,"roles":1839,"affiliations":1840,"properties":1849,"displayName":1853,"givenName":24,"familyName":24},"40ce97b1-2347-424f-9a02-bdab66ce31cf",[],[1841],{"id":1842,"sortIndex":25,"affiliation":1843,"properties":24},"3d594e8b-2d99-4895-b197-f9f20fef1741",{"id":1842,"createTime":24,"updateTime":24,"relativeEntities":1844,"slug":24,"properties":1845,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1848,"statistic":24},[],{"title":1846},{"EN":1847},"Dept. of Cellular and Molecular Physiology, Yale School of Medicine, New Haven, CT 06520-8026, USA.",[],{"orcid":1850,"title":1852,"openalex":1854},{"VOID":1851},"https:\u002F\u002Forcid.org\u002F0000-0001-7054-2540",{"EN":1853},"Tong Wang",{"VOID":1855},"A5100450969",{"id":1857,"sortIndex":101,"researcher":24,"roles":1858,"affiliations":1859,"properties":1860,"displayName":1862,"givenName":24,"familyName":24},"5322e0ee-1f0a-4248-9e79-97877f3ae16e",[],[],{"title":1861,"openalex":1863},{"EN":1862},"Hyacinth Sterling",{"VOID":1864},"A5112013541",{"id":1866,"sortIndex":104,"researcher":24,"roles":1867,"affiliations":1868,"properties":1869,"displayName":1871,"givenName":24,"familyName":24},"3b257e1a-603a-498a-8a19-f20575737b2d",[],[],{"title":1870,"openalex":1872},{"EN":1871},"Wei Shao",{"VOID":1873},"A5091400073",{"id":1875,"sortIndex":105,"researcher":24,"roles":1876,"affiliations":1877,"properties":1878,"displayName":1880,"givenName":24,"familyName":24},"007f19dd-2ed2-422f-93fc-568123813d27",[],[],{"title":1879,"openalex":1881},{"EN":1880},"Qingshang Yan",{"VOID":1882},"A5113549459",{"id":1884,"sortIndex":237,"researcher":24,"roles":1885,"affiliations":1886,"properties":1895,"displayName":1899,"givenName":24,"familyName":24},"bbb91233-d67d-4e9c-8281-2c456b8ec4ff",[],[1887],{"id":1888,"sortIndex":25,"affiliation":1889,"properties":24},"2b186401-b1b3-4df8-9218-a35d1341f45a",{"id":1888,"createTime":24,"updateTime":24,"relativeEntities":1890,"slug":24,"properties":1891,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":1894,"statistic":24},[],{"title":1892},{"EN":1893},"Deanery of Clinical Sciences",[],{"orcid":1896,"title":1898,"openalex":1900},{"VOID":1897},"https:\u002F\u002Forcid.org\u002F0000-0003-4244-5668",{"EN":1899},"Matthew A. 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Sodium chloride transport. In: The Kidney:  Physiology and Pathophysiology, edited by Seldin DW and Giebisch  G. New York: Raven, 1992, p.  2003-2039.",{},{"id":24,"text":2021,"url":24,"identifiers":2022},"10.1016\u002FS0014-2999(97)00057-5",{"doi":2021},{"id":24,"text":2024,"url":24,"identifiers":2025},"10.1038\u002Fki.1983.46",{"doi":2024},{"id":24,"text":2027,"url":24,"identifiers":2028},"10.1172\u002FJCI5206",{"doi":2027},{"id":24,"text":2030,"url":24,"identifiers":2031},"10.1152\u002Fajprenal.1985.248.5.F682",{"doi":2030},{"id":24,"text":2033,"url":24,"identifiers":2034},"10.1038\u002Fki.1978.146",{"doi":2033},{"id":24,"text":1487,"url":24,"identifiers":2036},{"doi":1487},{"id":24,"text":2038,"url":24,"identifiers":2039},"10.1111\u002Fj.1432-1033.1997.00725.x",{"doi":2038},{"id":24,"text":2041,"url":24,"identifiers":2042},"10.1016\u002F0896-6273(95)90222-8",{"doi":2041},{"id":24,"text":1744,"url":24,"identifiers":2044},{"doi":1744},{"id":24,"text":2046,"url":24,"identifiers":2047},"10.1038\u002Fng1097-171",{"doi":2046},{"id":24,"text":2049,"url":24,"identifiers":2050},"10.1038\u002Fng1096-152",{"doi":2049},{"id":24,"text":2052,"url":24,"identifiers":2053},"10.1038\u002Fki.1994.371",{"doi":2052},{"id":24,"text":1797,"url":24,"identifiers":2055},{"doi":1797},{"id":24,"text":2057,"url":24,"identifiers":2058},"10.1074\u002Fjbc.272.13.8222",{"doi":2057},{"id":24,"text":2060,"url":24,"identifiers":2061},"10.1007\u002Fs004240050398",{"doi":2060},{"id":24,"text":2063,"url":24,"identifiers":2064},"Wang T, Wang  WH, Klein-Robbenhaar T, and Giebisch G. Effects of glyburide on renal  tubule transport and potassium channel activity. Renal Physiol  Biochem 18:  169-182, 1995.",{"doi":2065},"10.1159\u002F000173914",{"id":24,"text":2067,"url":24,"identifiers":2068},"Wang T, Wang  WH, Klein-Robbenhaar T, and Giebisch G. Effects of a novel KATP channel  blocker on renal tubule function and K channel activity. J  Pharmacol Exp Ther 273:  1382-1389, 1995.",{},{"id":24,"text":2070,"url":24,"identifiers":2071},"10.1152\u002Fajprenal.00316.2001",{"doi":2070},{"id":24,"text":2073,"url":24,"identifiers":2074},"10.1152\u002Fajprenal.2000.279.1.F153",{"doi":2073},{"id":2076,"createTime":2077,"updateTime":2078,"relativeEntities":2079,"slug":2080,"properties":2081,"entityType":160,"verifyStatus":161,"verifyTime":2077,"verifyNote":162,"languages":2097,"translateLanguages":2098,"viewCount":25,"primaryUrl":2099,"fullTextUrl":24,"authors":2100,"publicationType":251,"publisherRelationship":2137,"citationCount":2190,"citationInfo":2191,"publishDate":2196,"publishYear":1043,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":2197,"openAccess":24,"references":2198,"isForceReanalyzing":316},"0dec417f-c160-4d22-b0de-963768815c0f","2025-01-28T13:19:31.940+00:00","2025-02-12T16:15:45.775+00:00",[],"Products-of-heme-oxygenase-and-their-potential-therapeutic-applications",{"mag":2082,"keywords":2084,"openalex":2085,"abstract":2087,"title":2090,"pm":2093,"doi":2095},{"VOID":2083},"2097732899",{"VI":869},{"VOID":2086},"W2097732899",{"EN":2088,"VI":2089},"\u003Cjats:p>Heme oxygenase 1 (HO-1) is induced in response to cellular stress and is responsible for converting the prooxidant heme molecule into equimolar quantities of biliverdin (BV), carbon monoxide (CO), and iron. BV is then converted to bilirubin (BR) by the enzyme biliverdin reductase. Experimental evidence suggests that induction of the HO system is an important endogenous mechanism for cytoprotection and that the downstream products of heme degradation, CO, BR, and BV, may mediate these powerful beneficial effects. These molecules, which were once considered to be toxic metabolic waste products, have recently been shown to have dose-dependent vasodilatory, antioxidant, and anti-inflammatory properties that are particularly desirable for tissue protection during organ transplantation. In fact, recent work has demonstrated that administration of exogenous CO, BR, or BV may offer a simple, inexpensive method to substitute for the cytoprotective effects of HO-1 in a variety of clinically applicable models. This review will attempt to summarize the relevant biochemical and cytoprotective properties of CO, BR, and BV, and will discuss emerging studies involving the therapeutic applications of these molecules in the kidney and other organ systems.\u003C\u002Fjats:p>","\u003Cjats:p>Heme oxygenase 1 (HO-1) được kích thích trong phản ứng với căng thẳng tế bào và có trách nhiệm chuyển đổi phân tử heme prooxidant thành các lượng tương đương biliverdin (BV), carbon monoxide (CO) và sắt. BV sau đó được chuyển đổi thành bilirubin (BR) bởi enzyme biliverdin reductase. Bằng chứng thực nghiệm cho thấy việc kích thích hệ thống HO là một cơ chế nội sinh quan trọng cho bảo vệ tế bào và rằng các sản phẩm downstream của sự phân hủy heme, CO, BR và BV, có thể trung gian cho các tác động tích cực mạnh mẽ này. Những phân tử này, vốn trước đây được coi là sản phẩm thải độc hại, gần đây đã được chứng minh có các tính chất giãn mạch, chống oxy hóa và chống viêm phụ thuộc vào liều, điều này đặc biệt mong muốn cho việc bảo vệ mô trong quá trình cấy ghép nội tạng. Thực tế, công trình gần đây đã chứng minh rằng việc sử dụng CO, BR hoặc BV ngoại sinh có thể cung cấp một phương pháp đơn giản và ít tốn kém để thay thế cho các tác động bảo vệ tế bào của HO-1 trong nhiều mô hình lâm sàng khác nhau. Bài tổng quan này sẽ cố gắng tóm tắt các đặc tính sinh hóa và bảo vệ tế bào liên quan của CO, BR và BV, và sẽ thảo luận về các nghiên cứu mới nổi liên quan đến các ứng dụng điều trị của những phân tử này trong thận và các hệ thống nội tạng khác.\u003C\u002Fjats:p>",{"EN":2091,"VI":2092},"Products of heme oxygenase and their potential therapeutic applications","Sản phẩm của heme oxygenase và ứng dụng trị liệu tiềm năng của chúng",{"VOID":2094},"16461755",{"VOID":2096},"10.1152\u002Fajprenal.00220.2005",[164],[778],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00220.2005",[2101,2118],{"id":2102,"sortIndex":25,"researcher":24,"roles":2103,"affiliations":2104,"properties":2113,"displayName":2115,"givenName":24,"familyName":24},"48ee64d4-2257-4d7b-890d-0d78381c8ddc",[],[2105],{"id":2106,"sortIndex":25,"affiliation":2107,"properties":24},"78f2c6f4-4138-4fd3-858c-a5631d9e6280",{"id":2106,"createTime":24,"updateTime":24,"relativeEntities":2108,"slug":24,"properties":2109,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2112,"statistic":24},[],{"title":2110},{"EN":2111},"The Comparative Nephrology and Transplantation Laboratory, Dept. of Small Animal Clinical Sciences, Veterinary Medical Teaching Hospital, PO Box 100126, Univ. of Florida, Gainesville, FL 32610-0126, USA.",[],{"title":2114,"openalex":2116},{"EN":2115},"Kristin A. 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published August 9, 2001; 10.1152\u002Fajprenal.00140.2001.—Heme oxygenase-1 (HO-1) catalyzes the rate-limiting step in heme degradation, releasing iron, carbon monoxide, and biliverdin. Induction of HO-1 occurs as an adaptive and protective response to several inflammatory stimuli. The transcription factor activator protein-1 (AP-1) has been implicated in the activation of the HO-1 gene. To elucidate the molecular mechanism of HO-1 induction, we examined the effects of diferuloylmethane (curcumin), an inhibitor of the transcription factor AP-1. Surprisingly, curcumin by itself was a very potent inducer of HO-1. Curcumin has anti-inflammatory, antioxidant, and renoprotective effects. To evaluate the mechanism of curcumin-mediated induction of HO-1, confluent human renal proximal tubule cells were exposed to curcumin (1–8 μM). We observed a time- and dose-dependent induction of HO-1 mRNA that was associated with increased HO-1 protein. Coincubation of curcumin with actinomycin D completely blocked the upregulation of HO-1 mRNA. Blockade of nuclear factor-κB (NF-κB) with an IκBα phosphorylation inhibitor attenuated curcumin-mediated induction of HO-1 mRNA and protein. These data demonstrate that curcumin induces HO-1 mRNA and protein in renal proximal tubule cells. HO-1 induction by curcumin is mediated, at least in part, via transcriptional mechanisms and involves the NF-κB pathway.\u003C\u002Fjats:p>","\u003Cjats:p>Được công bố lần đầu vào ngày 9 tháng 8 năm 2001; 10.1152\u002Fajprenal.00140.2001.—Heme oxygenase-1 (HO-1) xúc tác bước hạn chế tốc độ trong quá trình phân giải heme, giải phóng sắt, carbon monoxide và biliverdin. Sự kích thích HO-1 xảy ra như một phản ứng thích nghi và bảo vệ đối với một số tác nhân gây viêm. Yếu tố phiên mã protein hoạt hóa-1 (AP-1) đã được cho là có liên quan đến việc kích hoạt gen HO-1. Để làm sáng tỏ cơ chế phân tử của việc kích thích HO-1, chúng tôi đã kiểm tra tác động của diferuloylmethane (curcumin), một chất ức chế yếu tố phiên mã AP-1. Thật bất ngờ, curcumin tự nó lại là một tác nhân kích thích HO-1 rất mạnh. Curcumin có tác dụng chống viêm, chống oxy hóa và bảo vệ thận. Để đánh giá cơ chế kích thích HO-1 do curcumin điều hòa, các tế bào ống thận gần của người đã được tiếp xúc với curcumin (1–8 μM). Chúng tôi đã quan sát thấy sự kích thích mRNA HO-1 theo thời gian và liều lượng tương ứng với sự gia tăng protein HO-1. Sự đồng ấp giữa curcumin với actinomycin D hoàn toàn chặn lại sự tăng cường mRNA HO-1. Việc chặn yếu tố hạt nhân-κB (NF-κB) bằng chất ức chế phosphoryl hóa IκBα đã làm giảm sự kích thích mRNA và protein HO-1 do curcumin gây ra. Những dữ liệu này cho thấy curcumin kích thích mRNA và protein HO-1 trong các tế bào ống thận gần. Việc kích thích HO-1 do curcumin là do cơ chế phiên mã và liên quan đến con đường NF-κB.",{"EN":2565,"VI":2566},"Mechanism of heme oxygenase-1 gene induction by curcumin in human renal proximal tubule cells","Cơ chế kích thích gen heme oxygenase-1 bởi curcumin trong tế bào ống thận gần của người",{"VI":869},{"VOID":2569},"10.1152\u002Fajprenal.0140.2001",[164],[778],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.0140.2001",[2574,2593,2608,2625,2644],{"id":2575,"sortIndex":25,"researcher":24,"roles":2576,"affiliations":2577,"properties":2586,"displayName":2590,"givenName":24,"familyName":24},"58235673-9122-49bd-9080-e189a4dc1e7d",[],[2578],{"id":2579,"sortIndex":25,"affiliation":2580,"properties":24},"73889f1c-b857-48f1-a0fa-5f1a70c0d356",{"id":2579,"createTime":24,"updateTime":24,"relativeEntities":2581,"slug":24,"properties":2582,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2585,"statistic":24},[],{"title":2583},{"EN":2584},"Division of Nephrology, Hypertension and Transplantation, Department of Medicine,",[],{"orcid":2587,"title":2589,"openalex":2591},{"VOID":2588},"https:\u002F\u002Forcid.org\u002F0000-0002-9736-8885",{"EN":2590},"Nathalie Hill‐Kapturczak",{"VOID":2592},"A5044761237",{"id":2594,"sortIndex":101,"researcher":24,"roles":2595,"affiliations":2596,"properties":2603,"displayName":2605,"givenName":24,"familyName":24},"2d671753-6c60-40c2-80b9-34b2c27949a5",[],[2597],{"id":2579,"sortIndex":25,"affiliation":2598,"properties":24},{"id":2579,"createTime":24,"updateTime":24,"relativeEntities":2599,"slug":24,"properties":2600,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2602,"statistic":24},[],{"title":2601},{"EN":2584},[],{"title":2604,"openalex":2606},{"EN":2605},"Vijayalaksmi Thamilselvan",{"VOID":2607},"A5061666255",{"id":2609,"sortIndex":104,"researcher":24,"roles":2610,"affiliations":2611,"properties":2618,"displayName":2622,"givenName":24,"familyName":24},"e5c1869d-1f16-49ed-b24e-9796056ad412",[],[2612],{"id":2579,"sortIndex":25,"affiliation":2613,"properties":24},{"id":2579,"createTime":24,"updateTime":24,"relativeEntities":2614,"slug":24,"properties":2615,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2617,"statistic":24},[],{"title":2616},{"EN":2584},[],{"orcid":2619,"title":2621,"openalex":2623},{"VOID":2620},"https:\u002F\u002Forcid.org\u002F0000-0003-1007-1366",{"EN":2622},"Feiyan Liu",{"VOID":2624},"A5101964953",{"id":2626,"sortIndex":105,"researcher":24,"roles":2627,"affiliations":2628,"properties":2637,"displayName":2641,"givenName":24,"familyName":24},"acd98f0a-feba-485f-bb53-3893915aab43",[],[2629],{"id":2630,"sortIndex":25,"affiliation":2631,"properties":24},"7043c7c9-4000-4daf-84c2-2bdc99f0437d",{"id":2630,"createTime":24,"updateTime":24,"relativeEntities":2632,"slug":24,"properties":2633,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2636,"statistic":24},[],{"title":2634},{"VI":2635},"‖Department of Neuroscience, and",[],{"orcid":2638,"title":2640,"openalex":2642},{"VOID":2639},"https:\u002F\u002Forcid.org\u002F0000-0002-0374-2283",{"EN":2641},"Harry S. 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sản giật, podocyte, nephrin, podocalyxin, βig-h3, protein niệu, tổn thương thận",{"VOID":2928},"W2082398398",{"EN":2930,"VI":2931},"\u003Cjats:p>Emerging evidence has shown that podocyte injury and reduced specific podocyte protein expressions contribute to proteinuria in preeclampsia. We collected urine specimens from women with preeclampsia to study whether podocyte-specific protein shedding is associated with renal barrier dysfunction. Urine specimens from women with normal pregnancies and from pregnant women complicated by chronic hypertension were used for comparison. We determined soluble podocyte slit protein nephrin levels in the urine specimens. Podocalyxin, βig-h3, and VEGF concentrations were also measured. We found that nephrin and podocalyxin were barely detectable in the urine specimens from normal pregnant women and from women with chronic hypertension. In preeclampsia, urinary nephrin and podocalyxin concentrations were significantly increased and highly correlated to each other, r\u003Cjats:sup>2\u003C\u002Fjats:sup>= 0.595. Nephrin and podocalyxin were also correlated with urine protein concentrations. βig-h3 was detected in the urine specimens from women with preeclampsia, and it is highly correlated with nephrin and podocalyxin concentrations in preeclampsia. βig-h3 was undetectable in normal pregnancy and pregnancy complicated by chronic hypertension. Elevated VEGF levels were also found in women with preeclampsia compared with those of normal pregnancy and pregnancy complicated by chronic hypertension. These results provide strong evidence that podocyte protein shedding occurs in preeclampsia, and their levels are associated with proteinuria. The finding of urinary βig-h3 excretion in preeclampsia suggests that increased transforming growth factor activity might also be involved in the kidney lesion in this pregnancy disorder.\u003C\u002Fjats:p>","\u003Cjats:p>Các bằng chứng mới nổi đã chỉ ra rằng tổn thương tế bào podocyte và sự giảm biểu hiện các protein đặc hiệu của podocyte góp phần vào tình trạng protein niệu trong tiền sản giật. Chúng tôi đã thu thập mẫu nước tiểu từ phụ nữ mắc tiền sản giật để nghiên cứu xem việc thoát protein đặc hiệu của podocyte có liên quan đến sự rối loạn chức năng của hàng rào thận hay không. Các mẫu nước tiểu từ phụ nữ mang thai bình thường và từ những phụ nữ mang thai có mắc tăng huyết áp mãn tính được sử dụng để so sánh. Chúng tôi xác định nồng độ protein khe podocyte hòa tan nephrin trong các mẫu nước tiểu. Các nồng độ podocalyxin, βig-h3 và VEGF cũng được đo. Chúng tôi nhận thấy rằng nephrin và podocalyxin hầu như không thể phát hiện trong các mẫu nước tiểu từ phụ nữ mang thai bình thường và từ những phụ nữ mắc tăng huyết áp mãn tính. Trong tiền sản giật, nồng độ nephrin và podocalyxin trong nước tiểu tăng đáng kể và có sự tương quan cao với nhau, r\u003Cjats:sup>2\u003C\u002Fjats:sup>= 0.595. Nephrin và podocalyxin cũng có sự tương quan với nồng độ protein trong nước tiểu. βig-h3 đã được phát hiện trong các mẫu nước tiểu từ phụ nữ mắc tiền sản giật và có sự tương quan cao với nồng độ nephrin và podocalyxin ở tiền sản giật. βig-h3 không thể phát hiện trong thai kỳ bình thường và thai kỳ mắc tăng huyết áp mãn tính. Nồng độ VEGF cũng tăng cao ở phụ nữ mắc tiền sản giật so với những người mang thai bình thường và mang thai có mắc tăng huyết áp mãn tính. Những kết quả này cung cấp bằng chứng mạnh mẽ rằng việc thoát protein podocyte xảy ra trong tiền sản giật, và các mức độ của chúng liên quan đến protein niệu. Việc phát hiện sự bài tiết βig-h3 trong nước tiểu ở bệnh nhân tiền sản giật cho thấy rằng hoạt tính của yếu tố tăng trưởng chuyển đổi có thể cũng liên quan đến tổn thương thận trong rối loạn thai kỳ này.\u003C\u002Fjats:p>",{"EN":2933,"VI":2934},"Increased urinary excretion of nephrin, podocalyxin, and βig-h3 in women with preeclampsia","Tăng cường bài tiết nước tiểu của nephrin, podocalyxin và βig-h3 ở phụ nữ mắc tiền sản giật",{"VOID":2936},"22301621",{"VOID":2938},"10.1152\u002Fajprenal.00597.2011","2025-02-02T23:34:37.468+00:00",[164],[778],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajprenal.00597.2011",[2944,2971,2988,3003],{"id":2945,"sortIndex":25,"researcher":24,"roles":2946,"affiliations":2947,"properties":2964,"displayName":2968,"givenName":24,"familyName":24},"08409576-b632-425f-a276-f33cbed41fc6",[],[2948,2956],{"id":2949,"sortIndex":25,"affiliation":2950,"properties":24},"6fe92983-27f2-4654-8e56-29ba35e982f2",{"id":2949,"createTime":24,"updateTime":24,"relativeEntities":2951,"slug":24,"properties":2952,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2955,"statistic":24},[],{"title":2953},{"EN":2954},"Departments of 1Obstetrics and Gynecology and",[],{"id":2957,"sortIndex":101,"affiliation":2958,"properties":24},"cced7cad-5567-48a7-aa4c-77019c06a223",{"id":2957,"createTime":24,"updateTime":24,"relativeEntities":2959,"slug":24,"properties":2960,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2963,"statistic":24},[],{"title":2961},{"EN":2962},"Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, Shreveport, Louisiana",[],{"orcid":2965,"title":2967,"openalex":2969},{"VOID":2966},"https:\u002F\u002Forcid.org\u002F0000-0002-8676-7549",{"EN":2968},"Yuping Wang",{"VOID":2970},"A5100339118",{"id":2972,"sortIndex":101,"researcher":24,"roles":2973,"affiliations":2974,"properties":2981,"displayName":2985,"givenName":24,"familyName":24},"66ad2b2b-f10a-4f45-b182-da408d401d82",[],[2975],{"id":2949,"sortIndex":25,"affiliation":2976,"properties":24},{"id":2949,"createTime":24,"updateTime":24,"relativeEntities":2977,"slug":24,"properties":2978,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2980,"statistic":24},[],{"title":2979},{"EN":2954},[],{"orcid":2982,"title":2984,"openalex":2986},{"VOID":2983},"https:\u002F\u002Forcid.org\u002F0000-0001-7081-6177",{"EN":2985},"Shuang Zhao",{"VOID":2987},"A5031061480",{"id":2989,"sortIndex":104,"researcher":24,"roles":2990,"affiliations":2991,"properties":2998,"displayName":3000,"givenName":24,"familyName":24},"6dc2bab0-75b2-4938-bf23-96c066412bbd",[],[2992],{"id":2949,"sortIndex":25,"affiliation":2993,"properties":24},{"id":2949,"createTime":24,"updateTime":24,"relativeEntities":2994,"slug":24,"properties":2995,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":2997,"statistic":24},[],{"title":2996},{"EN":2954},[],{"title":2999,"openalex":3001},{"EN":3000},"Susan Loyd",{"VOID":3002},"A5005894125",{"id":3004,"sortIndex":105,"researcher":24,"roles":3005,"affiliations":3006,"properties":3013,"displayName":3015,"givenName":24,"familyName":24},"74988885-2afe-4b39-8cfd-decab04cef03",[],[3007],{"id":2949,"sortIndex":25,"affiliation":3008,"properties":24},{"id":2949,"createTime":24,"updateTime":24,"relativeEntities":3009,"slug":24,"properties":3010,"entityType":24,"verifyStatus":24,"verifyTime":24,"verifyNote":24,"languages":24,"translateLanguages":24,"viewCount":24,"url":24,"parentIds":3012,"statistic":24},[],{"title":3011},{"EN":2954},[],{"title":3014,"openalex":3016},{"EN":3015},"Lynn J. 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