安徽医科大学学报2019，Vol.54Issue(1)：50-55,6.DOI:10.19405/j.cnki.issn1000-1492.2019.01.010
低氧损伤下调大鼠脑血管内皮细胞中硫化氢及其介导的Rho A-ROCK通路激活
Anoxic injury down-regulates hydrogen sulfide in rat cerebrovascular endothelial cells and H2S-mediated activation of RhoA-ROCK pathway
摘要
Abstract
Objective To observe the effect of different hypoxic time on hydrogen sulfide (H2S), nitric oxide (NO) and Ras homolog gene family,member A/Rho associated coiled coil-forming kinase(RhoA-ROCK) pathway in rat cerebrovascular endothelial cells(EC),and investigate the effect of dermatogenous H2S on the RhoA-ROCK pathway. Methods Rat brain vascular EC was cultured by collagenase digestion. The EC was measured for H2S and NO after hypoxia for 1,2,4,8 and 24 h respectively. G-LISA was used to detect RhoA activity. Proteins expression changes were detected by Western blot. Results After 1 hour of hypoxia,the content of H2S decreased significantly, the NO content decreased significantly after hypoxia of 4 hours,the activity of RhoA increased significantly after hypoxia of 8 h. The expression of CSE protein decreased significantly after 4 h of hypoxia,the expression level of eNOS protein decreased significantly after 8 h of hypoxia,and the expression of ROCK1 and ROCK2 increased significantly at 8 h of hypoxia. Both endogenous and exogenous H2S inhibited RhoA activity. Conclusion During the hypoxic injury of rat cerebrovascular endothelial cells. The decrease of endogenous H2S occurred first, followed by NO,and the activation of RhoA-ROCK pathway occurred later,which may be secondary to the decrease of H2S.关键词
内皮细胞/低氧/硫化氢/RhoA-ROCK通路Key words
endothelial cell/hypoxia/hydrogen sulfide/RhoA-ROCK pathway分类
医药卫生引用本文复制引用
王良芳,陈志武..低氧损伤下调大鼠脑血管内皮细胞中硫化氢及其介导的Rho A-ROCK通路激活[J].安徽医科大学学报,2019,54(1):50-55,6.基金项目
国家自然科学基金(编号:81374002) （编号:81374002）
