Hydroxy-safflower yellow A improves mitochondrial dysfunction in myocardial ischemia reperfusion injury by regulating SIRT3
Objective To investigate the protective effect of hydroxy-safflower yellow A(HSYA)on the mitochondrial function in the myocardial cell line H9c2 induced by lipopolysaccharide(LPS)and its regulation on SIRT3.Methods H9c2 cells were cultured for 24 h,and treated with control,LPS induction,LPS induction+SIRT3 inhibitor,HSYA+LPS induction,and HSYA+LPS induction+SIRT3 inhibitor.LPS induction was performed in H9c2 cells to create the in vitro oxidative stress model in cardiomyocytes.Lactate dehydrogenase detection kit was used to determine the content of lactate dehydrogenase in the culture medium.The contents of adenosine triphosphate(ATP),cytochrome C and mitochondrial respiratory chain complex in cells were measured.The protein expressions of SIRT3 and Bax were detected by Western blot.Results Compared with those treated with control,LPS induction significantly increased the contents of cytochrome C and glutamate dehydrogenase in cells,and significantly decreased ATP and respiratory chain complex.Meanwhile,LPS induction slightly upregulated SIRT3 and significantly upregulated Bax.Compared with those induced with LPS,mitochondrial dysfunction indicators were significantly pronounced in LPS-induced H9c2 cells treated with SIRT3 inhibitor,which were significantly reversed by the treatment of HSYA.The degree of mitochondrial dysfunction was lower in H9c2 cells treated with LPS+HSYA+SIRT3 inhibitor than those treated with LPS+SIRT3 inhibitor,and SIRT3 was upregulated in the former group.Conclusion HSYA can reduce mitochondrial oxidative damage in LPS-induced H9c2 cells by upregulating SIRT3 in injured cardiomyocytes.
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