Apigenin Alleviates Palmitic Acid-induced Cardiomyocytes Apoptosis by Upregulating Quaking Expression
Objective To explore the role and mechanism of apigenin(APi)in palmitate acid(PA)-induced apoptosis in H9C2 cardiomyocytes.Methods APi(or QKI overexpression)intervened in PA-induced apoptosis of H9C2 cardiomyocytes;West-ern Blot was performed to detect protein expression in cells;Intracellular calcium concentration was determined by Fluo-4AM.Results 10μmol/L APi had the best effect on PA-induced Cleaved-caspase 3 protein expression in H9C2 cardiomyocytes,and the inhibitory effect was gradually weakened as the concentration of APi increased.The intervention of APi significantly inhibited the PA-induced down-regulation of QKI,SERCA2α,RyR2 expression and up-regulation of Cleaved-caspase 3 protein expression.Simil-ary,overexpression of QKI significantly inhibited the PA-induced down-regulation of QKI,SERCA2α,RyR2 expression and up-reg-ulation of Cleaved-caspase 3 protein expression.The intervention of APi(or QKI overexpression)alleviated the PA-induced in-crease in calcium concentration in H9C2 cardiomyocytes.Conclusion APi promotes the expression of QKI in cardiomyocytes,there-by maintaining intracellular Ca2+dynamic balance and improving PA-induced cardiomyocyte apoptosis.
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