Roles of heat shock protein 90 in the blockage of H2S against cardiomyocyte injuries induced by chemical hypoxia
- VernacularTitle:热休克蛋白90在硫化氢抗化学性缺氧诱导心肌细胞氧化应激损伤中的作用
- Author:
Shuisheng WEI
;
Xinxue LIAO
;
Yupin TAN
;
Zhanli YANG
;
Chuntao YANG
;
Chunmei ZHAO
;
Xiaobian DONG
;
Lichun WANG
;
Peixi CHEN
;
Jianqiang FENG
- Publication Type:Journal Article
- Keywords:
Heat-shock proteins 90;
Hydrogen sulfide;
Cobalt chloride;
Cardiomyocytes;
Oxidative stress
- From:
Chinese Journal of Pathophysiology
2009;25(12):2329-2333
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To explore the roles of heat shock protein 90 (HSP90) in the blockage of hydrogen sulfide (H2S) against chemical hypoxia-mimetic agent (cobalt chloride, CoCl_2)-induced oxidative stress injuries in H9c2 cardiac cell. METHODS: H9c2 cells were treated with CoCl_2 to set up the chemical hypoxia-induced the model of cardiomyocyte injury. Sodium hydrosulfide (NaHS, a H2S donor) was added into medium for 30 min before CoCl_2 treatment. ATP content was detected by high performance liquid chromatogram (HPLC). Mitochondrial membrane potential (MMP) was measured by rhodamine123 (Rh123) staining and photofluorography. The activity of superoxide dismutase (SOD) was observed using a SOD kit. The expression of heme oxygenase-1 (HO-1) was evaluated by Western blotting. RESULTS: CoCl_2 at concentration of 600 μmol/L significantly reduced SOD activity, ATP level and MMP, and enhanced the expression of HO-1 in H9c2 cells. Pretreatment with 400 μmol/L NaHS dramatically inhibited the cytotoxicity induced by CoCl_2, increased SOD activity, ATP level and MMP, decreased HO-1 expression. 17-allylamino-17 demethoxygeldanamycine(17AAG), an inhibitor of HSP90, obviously blocked the inhibitory effect of H2S on the CoCl_2-induced cytotoxicity, reduced the levels of ATP and MMP, increased HO-1 expression. However, no significantly influence on SOD activity was observed. CONCLUSION: HSP90 may mediate the cardioprotection of H2S via inhibiting the oxidative stress induced by chemical hypoxia.
