Key result
Si-Miao-Yong-An decoction improved cardiac function, reduced scar size, and protected cardiomyocytes from ischemia/reperfusion injury by activating autophagy and inhibiting pyroptosis.
Why the study?
It was unknown whether Si-Miao-Yong-An decoction protects cardiomyocytes from ischemia/reperfusion injury and what underlying mechanisms are involved.
Does Si-Miao-Yong-An decoction improve cardiac function and protect against ischemia/reperfusion injury in C57BL/6 mice and H9C2 cells?
Does Si-Miao-Yong-An decoction improve cardiac function and protect against ischemia/reperfusion injury in C57BL/6 mice and H9C2 cells?
Si-Miao-Yong-An decoction protects against myocardial ischemia/reperfusion injury by activating autophagy and inhibiting pyroptosis in preclinical models.
Objective. The aim of this study was to determine whether Si-Miao-Yong-An decoction (SMYAD) could protect cardiomyocytes from ischemia/reperfusion (I/R) injury and its underlying mechanisms. Methods. C57BL/6 mice were used to establish a model of myocardial infarction by I/R injury and treated by SMYAD for 4 weeks. Then, the cardiac functions of mice were evaluated by cardiac magnetic resonance (CMR). Histopathological analysis for the heart remodeling was detected by H&E and Masson staining. The protein expression of collagen I, MMP9, and TNFα was detected by western blot in the heart tissues. H9C2 cells were used to establish the hypoxia/reoxygenation (H/R) model and SMYAD intervention. MTT assays detected the cell viability of myocardial cells. The expression level of IL-1β was evaluated by ELISA. The expression levels of LC3B-II/LC3B-I, p-mTOR, mTOR, NLRP3, procaspase 1, and cleaved-caspase 1 in H9C2 cells were evaluated by Western blot. Results. SMYAD improved cardiac functions such as ventricular volume and ejection fraction of the rats with ischemia/reperfusion injury. Morphological assay indicated that SMYAD reduced the scar size and inhibited fibrosis formation. It was found that SMYAD could regulate collagen I, MMP9, and TNFα protein expression levels in the heart tissues. SMYAD improved the survival rate of H9C2 cardiomyocytes in the H/R injury model. SMYAD elevated the rate of LC3B-II/LC3B-I protein expression, decreased the rate of p-mTOR/mTOR protein expression, and reduced expressions of caspase 1, NLRP3, and IL-1β in H/R cardiomyocytes. Conclusion. SMYAD exerted protective effects on ischemia/reperfusion injury in myocardial cells by activating autophagy and inhibiting pyroptosis. This might be the reason why SMYAD protected myocardial tissue and improved cardiac function in mice with ischemia/reperfusion.
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Cui et al. (2021) studied Myocardial ischemia and reperfusion injury. Si-Miao-Yong-An decoction (SMYAD) was evaluated on Cardiac function and cell viability. Si-Miao-Yong-An decoction improved cardiac function, reduced scar size, and protected cardiomyocytes from ischemia/reperfusion injury by activating autophagy and inhibiting pyroptosis.
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