Anoxic injury down-regulates hydrogen sulfide in rat cerebrovascular endothelial cells and H2S-mediated activation of RhoA-ROCK pathway / 安徽医科大学学报

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.