RESUMO
Objective To investigate the cytoprotection and mechanism of carbachol(CCH)to stimulate M3mus-carinic acetylcholine receptor(M3-mAChR) against hypoxia injury induced by cobaltous chloride hexahydrate (CoCl2) in rat cardiomyocyte line H9c2. Methods Select the normal rat cardiomyocyte line H9c2 as the control group, rat cardiomyocyte line H9c2 was managed with CoCl2to develop hypoxia injury model, M3-mAChR spe-cific agonist CCH and antagonist 4-diphenyl-acetoxy-N-methyl-piperidine methiodide(4-DAMP) were used for in-tervention. The cell viability was tested by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT); The apoptosis in cardiomyocyte was detected by flow cytomery(FCM); The expression of M3-mAChR,caspase-3, HIF-1α and HO-1 proteins was measured by Western blot assay. Results In hypoxia group,the ap-optosis rate was significantly increased while cell proliferation decreased, the expression of HIF-1α, caspase-3 and HO-1 proteins were up-regulated obviously;After treatment with CCH,the apoptosis and cell proliferation of cardiomyocytes were significantly decreased, while the proliferation of cells increased, and the expression of M3-mAChR, HIF-1α and HO-1 proteins increased, the expression of caspase-3 protein was significantly decreased. Moreover, when applying 4-DAMP as intervention, these effects mediated by CCH was abolished.Conclusions CCH stimulates M3-mAChR against hypoxia injury induced by CoCl2in rat cardiomyocyte strain H9c2, and the mechanism may be related to down-regulation of caspase-3 expression and up-regulation of HIF-1α and HO-1 protein expression.