Mechanism involved in damp-heat induced mice myocardial cell apoptosis

Objective To explore the mechanism of damp-heat induced mice myocardial cell apoptosis.Methods In this study,mice was exposed to damp-heat(42℃,RH 65%)(H group) environment or room temperature(C group).The myocardial cell apoptosis rates in tissues were analyzed by TUNEL staining.The expression levels of Ang Ⅱ were detected by EIISA assay.Cardiomyocytes of rats with 1 day were pretreated with caspase-3 inhibitor ZDEVD-FMK,or P38 MAPK inhibitor SB203580,for 24 h,followed by culturing with the indicated dose of AngⅡ.AnnexinV-FITC was used to analyze cell apoptosis ratio.In addition,the expression of caspase-3 and P38MAPK was assessed by Western blot.Results The rates of cell apoptosis and Ang Ⅱ expression levels in H group were significantly higher than those in C group(P0.05).In vitro,Ang Ⅱ dose-dependently induced cardiomyocytes apoptosis,accompany with the up-regulation of caspase-3 and P38 MAPK expression.When preconditioning with Z-DEVD-FMK,the apoptotic ratio of cardiomyocytes was significantly attenuated in Ang Ⅱ-treated group,implying that Ang Ⅱ triggered cell apoptosis in caspase-3-depedent manner.Additionally,pretreatment with SB203580 dramatically abrogated caspase-3 expression induced by Ang Ⅱ.Conclusions Damp-heat environment induced cardiomyocytes apoptosis by Ang Ⅱ-activated P38 MAPK-caspase-3 pathway.Consequently,Ang Ⅱ may be a potential target for innovative strategies against cardiovascular diseases induced by Damp-heat environment.