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Protective effects of icariin on human umbilical vein endothelial cell injured by angiotensin Ⅱ 被引量:3

淫羊藿苷对血管紧张素Ⅱ诱导人脐静脉内皮细胞损伤的保护作用(英文)
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摘要 To investigate the effects of icariin (ICA) on angiotensin Ⅱ(Ang Ⅱ)-induced injury in human umbilical vein endothelial cells line (ECV-304). The ECV-304 cells were cultured in vitro. After 24 h incubating with icariin, the model of AngⅡ-induced injury in ECV-304 was established. The cell viability (MTT method), Lactate dehydrogenase (LDH) release and Nitric oxide (NO) production in the medium, the capacity of scavenging superoxide anion radicals (O2^-) and hydroxyl radicals (.OH) were measured. The activities of superoxide dismutase (SOD), total nitric oxide synthase (T-NOS), inducible nitric oxide synthase (iNOS) and constitutive nitric oxide synthase (cNOS) in the cells were determined. Compared with the Ang Ⅱ-treated group, ICA can significantly raise the viability of EC, increase the activities of SOD, T-NOS and cNOS, increase the production of NO, enhance the capacity of scavenging superoxide anion radicals ( O2^- ) and hydroxyl radicals(.OH), and lower LDH leakage and iNOS activity. The results suggest that ICA can protect endothelial cells (ECV-304) from Ang II-induced injury. 探讨淫羊藿苷对血管紧张素Ⅱ(AngⅡ)诱导损伤人脐静脉内皮细胞株(ECV-304)的影响。培养内皮细胞,淫羊藿苷作用24h后,采用AngⅡ诱导制备内皮细胞损伤模型,测定细胞存活率(MTT法)、培养液中乳酸脱氢酶(LDH)释放量、NO值、清除超氧阴离子自由基(O2g-)和羟自由基(·OH)的能力,测定胞内超氧化物歧化酶(SOD)活性、T-NOS﹑iNOS以及cNOS的含量。与AngⅡ单独处理组相比,淫羊藿苷能明显提高细胞存活率,提高SOD、T-NOS和cNOS活力,提高NO含量,增强清除O2g-和·OH的能力,降低LDH和iNOS的量。结果表明淫羊藿苷对AngⅡ损伤的内皮细胞有一定的保护作用。
出处 《Journal of Chinese Pharmaceutical Sciences》 CAS 2008年第1期16-21,共6页 中国药学(英文版)
基金 National "Ninth five-year" Key Technology R&D Programme of China (Grant No.99-929-01-31)
关键词 ICARIIN Angiotensin Human umbilical vein endothelial cells line Nitric oxide 淫羊藿苷 血管紧张素Ⅱ 人脐静脉内皮细胞株(ECV-304) 一氧化氮
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  • 1Sho-ichi Yamagishi,Kazuo Nakamura,Seiji Ueda,Seiya Kato,Tsutomu Imaizumi. Pigment epithelium-derived factor (PEDF) blocks angiotensin II signaling in endothelial cells via suppression of NADPH oxidase: a novel anti-oxidative mechanism of PEDF[J] 2005,Cell and Tissue Research(3):437~445

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