Abstract: Objective To explore the mechanism of damp-heat induced mice myocardial cell apoptosis. Method 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 Z-DEVD-FMK, or p38MAPK inhibitor SB203580, for 24 h, followed by culturing with the indicated dose of Ang II. AnnexinV-FITC was used to analyze cell apoptosis ratio. In addition, the expression of caspase-3 and p38MAPK was assessed by Western blotting. Results The rates of cell apoptosis and Ang II expression levels in H group were significantly higher than those in C group (P<0.05). 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. Conclusion Damp-heat environment induced cardiomyocytes apoptosis by Ang II-activated p38MAPK-caspase-3 pathway. Consequently, Ang II may be a potential target for innovative strategies against cardiovascular diseases induced by Damp-heat environment.

Key words: damp-heat stress, Angiotensin II, apoptosis, p38 MAPK, caspase-3