Exogenous H(2)S Protects against Septic Cardiomyopathy by Inhibiting Autophagy through the AMPK/mTOR Pathway

BACKGROUND: Given the cardioprotective role of autophagy, this study aimed to investigate the protective effect of exogenous H(2)S (NaHS) on infectious cardiomyopathy through the inhibition of the AMPK/mTOR pathway. METHODS: In this study, sepsis models were established by cecal ligation and puncture (CLP) induction in vivo and intraperitoneal injection of NaHS was performed. Autophagy- and apoptosis-related proteins were observed by western blot, isolated myocardial tissue morphology was observed by hematoxylin-eosin (H&E) staining, and myocardial apoptosis was evaluated by the tunnel method. The ultrastructure of autophagy was observed by using an electron transmission electron microscope. RESULTS: In an SD rat model of cecum ligation puncture-induced sepsis, the level of autophagy-related proteins was significantly increased, and hematoxylin and eosin staining showed irregular myocardial bands and swollen cardiomyocytes. Following NaHS treatment, the level of autophagy-related proteins decreased, and electron transmission microscopy revealed decreased autophagosomes. Echocardiography suggested an increase in ejection fraction and significant relief of myocardial inhibition. CONCLUSIONS: Our results suggest that NaHS treatment can attenuate the cellular damage caused by excessive autophagy through the AMPK/mTOR pathway.