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Updated: Sep 5, 2025

Cecal Ligation and Puncture-induced Sepsis as a Model To Study Autophagy in Mice
Published on: February 9, 2014
Exogenous H2S Protects against Septic Cardiomyopathy by Inhibiting Autophagy through the AMPK/mTOR Pathway
YuHan Zhao1, QingHong Cheng1,2
1Shihezi University School of Medicine, Shihezi 832000, China.
Background:
Given the cardioprotective role of autophagy, this study aimed to investigate the protective effect of exogenous H2S (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.
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