AIM To investigate whether saponins extracted from Aralia taibaiensis (sAT) can inhibit myocardial damage and cardiomyocyte pyroptosis caused by endotoxin (LPS).
METHODS Male C57/BL6 mice were randomly divided into normal control group, sAT control group, LPS group and LPS+sAT group, with 8 mice in each group. C57/BL6 mice were treated with sAT 240 mg/(kg·d) for 7 days, followed by intraperitoneal injection of LPS (15 mg/kg) for 24h. Cardiac functions and inflammatory factors were measured and cardiac caspase-11 was detected by Western blot. In cytology experiments, H9C2 cardiomyocytes were used to establish cell pyroptosis model induced by LPS combined with cholera toxin B-type subunit (CTB). The effect of sAT on the survival rate of H9C2 cells and the levels of IL-1β, LDH levels and caspase-11 was measured.
RESULITS LPS caused significant cardiac dysfunction, increased plasma CK-MB level, significantly increased mortality and marked increased in inflammatory response in myocardial tissue compared with those in control group (P < 0.05). sAT treatment alleviated cardiac dysfunction, inhibited inflammatory response and decreased mortality in LPS group compared with those in LPS group (P < 0.05). LPS resulted in pyroptosis in myocardial tissue, which was characterized by myocardial caspase-11 activation, elevated IL-1β level and plasma LDH level. sAT treatment effectively inhibited myocardial pyroptosis caused by LPS. Cytological experiments confirmed that LPS combined with CTB induced the pyroptosis of H9C2 cardiomyocytes. sAT treatment effectively inhibited the activation of caspase-11, reduced the levels of IL-1β and LDH in cell culture supernatant, and significantly improved H9C2 cardiomyocytes survival rate.
CONCLUSION sAT attenuates LPS induced myocardial injury and cardiac dysfunction and effectively inhibits myocardial pyroptosis.
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