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中国临床药理学与治疗学 ›› 2003, Vol. 8 ›› Issue (4): 381-384.

• 研究原著 • 上一篇    下一篇

金粉蕨素拮抗血管内皮细胞氧化应激损伤及机制1

庹勤慧, 廖端芳, 朱炳阳, 严奉祥   

  1. 南华大学基础医学院药物药理研究所,衡阳 421001,湖南
  • 收稿日期:2003-02-21 修回日期:2003-03-01 出版日期:2003-08-26 发布日期:2020-11-19
  • 通讯作者: 廖端芳,博士,教授,博士生导师,研究方向:心血管药理学。Tel:0734-8281308  E-mail:dfliao@hotmail.com
  • 作者简介:庹勤慧,在读硕士研究生。E-mail:qhtuo@sohu.com 。
  • 基金资助:
    1 卫生部资助课题(No981345);湖南省中医药科研基金重点课题(No2000006);湖南省教委资助课题(No98B100)

Protective effects of onychin on vascular endothelial cell injured by oxidative stress1

TUO Qin-Hui, lIAO Duan-Fang, ZHU Bing-Yang, YAN Feng-Xiang   

  1. Institute ofPharmacy&Pharmacology,Nanhua University,Hengyang 421001,Hunan,China
  • Received:2003-02-21 Revised:2003-03-01 Online:2003-08-26 Published:2020-11-19

摘要: 目的 研究金粉蕨素(onychin,Ony)对血管内皮细胞氧化应激损伤的影响及可能机制。方法 培养人脐静脉血管内皮细胞株(ECV304),经Ony 处理后,用过氧化氢(H2O2)对其损伤;用MTT 比色法和乳酸脱氢酶测定法分别检测损伤组和处理组细胞增殖活性和功能状态;用Western-Blot 法检测磷酸化ERK1/2 和p38 、P90RSK 蛋白的表达。结果 不同浓度的Ony(0.3 、1 、3 、10μmol·L-1)促进H2O2损伤的内皮细胞增殖,减少LDH 释放,并呈浓度依赖性。Ony(3μmol·L-1)抑制H2O2诱导的磷酸化p38 表达,30 min 时最明显,但并不影响H2O2对ERK 的激活以及ERK 下游蛋白激酶P90RSK 的表达。而阳性对照药genistein 虽可增加内皮细胞增殖活性和减少功能损伤,但明显抑制H2O2诱导的磷酸化ERK 表达及其下游蛋白激酶P90RSK 。结论 Ony 拮抗血管内皮细胞氧化应激损伤可能与抑制p38 磷酸化有关。

关键词: 药理学, 金粉蕨素, 内皮细胞, 过氧化氢, ERK, P38MAPK

Abstract: AIM: To study theProtective effects and mechanism of onychin against vascular endothelial cell damage induced by oxidative stress.METHODS: Cultured human umbilical vein endothelial cells(ECV304)and incubated them for 30 min with either vehicle(DMSO),genistein or different concentrations of onychin(0.1,0.3,1,3,and 10μmol·L-1)before being damaged with 2 mmol·L-1 H2O2.Cell viability was measured by the MTT assay andlDH assay,and cell morphologic changes were determined under microscope.Meanwhile,and the western blot was used to measure the expression ofPhospho-ERK,P90RSK,andPhospho-p38 of endothelial cells.RESULTS: Different doses of onychin obviously inhibited cell viability and increasedlDH release(P<0.01).Onychin(0.3,1,and 3μmol·L-1)improved the cellProliferation with the growth rate from 73.4 % to 82.9 %,90.1 % and 95.2 %,respectively.Onychin also attenuated the release of lDH(H2O2-induced)and inhibited H2O2-inducedPhosphorylation ofP38MAPK(P<0.01).Onychin showed no effect onPhosphorylation of ERK andP90RSK.CONCLUSION: OnychinPrevents H2O2-induced endothelial cell injury by inhibiting thePhosphorylation ofP38 MAPK.

Key words: pharmacology, onychin, endothelial cells, hydrogenPeroxide, p38 MAPK, ERK

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