Anoxic injury down-regulates hydrogen sulfide in rat cerebrovascular endothelial cells and H2S-mediated activation of RhoA-ROCK pathway
10.19405/j.cnki.issn1000-1492.2019.01.010
- VernacularTitle: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
- Author:
Liangfang WANG
1
;
Zhiwu CHEN
Author Information
1. 安徽医科大学药理学教研室
- Keywords:
endothelial cell;
hypoxia;
hydrogen sulfide;
RhoA-ROCK pathway
- From:
Acta Universitatis Medicinalis Anhui
2019;54(1):50-55
- CountryChina
- Language:Chinese
-
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.
