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KMID : 0811720230270040345
Korean Journal of Physiology & Pharmacology
2023 Volume.27 No. 4 p.345 ~ p.356
Hydrogen sulfide ameliorates abdominal aorta coarctation-induced myocardial fibrosis by inhibiting pyroptosis through regulating eukaryotic translation initiation factor 2¥á phosphorylation and activating PI3K/AKT1 pathway
Yaling Li

Lee Jong-Wook
Jiangping Hu
Gongli Liu
Hongming Hu
Fan Ouyang
Jun Yan
Abstract
This study aimed to assess the effects of exogenous hydrogen sulfide (H2S) on abdominal aorta coarctation (AAC) induced myocardial fibrosis (MF) and autophagy in rats. Forty-four Sprague?Dawley rats were randomly divided into control group, AAC group, AAC + H2S group, and H2S control group. After a model of rats with AAC was built surgically, AAC + H2S group and H2S group were injected intraperitoneally with H2S (100 ¥ìmol/kg) daily. The rats in the control group and the AAC group were injected with the same amount of PBS. We observed that H2S can improve left ventricular function and the deposition of myocardial collagen fibers, inhibit pyroptosis, down-regulate the expression of P-eif2¥á in myocardial tissue, and inhibit cell autophagy by activating the phosphatidylinositol 3-kinase (PI3K)/AKT1 signaling pathway (p < 0.05). In addition, angiotensin II (1 ¥ìM) H9c2 cardiomyocytes were injured in vitro experiments, and it was also observed that pyroptosis was inhibited after H2S (400 ¥ìmol/kg) intervention, the expression of P-eif2¥á in cardiomyocytes was significantly down-regulated, and the PI3K/AKT1 signaling pathway was activated at the same time. Therefore, increasing the expression of P-eif2¥á reverses the activation of the PI3K/AKT1 signaling pathway by H2S. In conclusion, these findings suggest that exogenous H2S can ameliorate MF in rats with AAC by inhibiting pyroptosis, and the mechanism may be associated with inhibiting the phosphorylation of eif2¥á and activating the PI3K/AKT1 signaling pathway to inhibit excessive cell autophagy.
KEYWORD
Fibrosis, Hydrogen sulfide, Phosphatidylinositol 3-Kinase, Phosphorylation, Pyroptosis
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