Objective To investigate whether flurbiprofen can reduce oxidative stress-induced cardiomyocyte injury and its specific mechanism.Methods The oxidative stress injury model of myocardial H9c2 cells was established and divided into Control group,H2O2 group,F+H2O2 group,F group,F+H2O2+Wort group,and Wort group.The cell activity was measured by MTT.The expression of anti-proliferating pro-teins PHB1 and PHB2,phosphorylated glycogen synthetase kinase-3β(p-GSK-3β)and phosphorylated pro-tein kinase-B(p-AKT)were detected by Western blot.Using laser confocal microscopy to observe mitochon-drial membrane potential.Results Compared with the H2O2 group,the F+H2O2(10,50,100μmol/L)group showed a statistically significant difference(P＜0.05).Compared with the H2O2 group,the difference of mitochondrial membrane potential level in the F+H2O2 group was statistically significant(P＜0.05);the decrease in the mitochondrial membrane potential level in the F+H2O2+Wort group compared with the F+H2O2 group was statistically significant(P＜0.05).Compared with the H2O2 group,p-GSK-3β,p-AKT and PHB2 were increased in the F+H2O2 group(P＜0.05);but PHB1 was unchanged in the F+H2O2 group(P＞0.05).Compared with the F+H2O2 group,PHB2,p-GSK-3β,and p-AKT proteins in the F+H2O2+Wort group were statistically significant(P＜0.05);however,PHB1 protein was unchanged in the F+H2O2+Wort group(P＞0.05).Conclusion Flurbiprofen may alleviate cardiac H9c2 cell oxidative dam-age induced mitochondrial permeablity transition pore(mPTP)opening by inhibiting GSK-3β and increasing PHB2 via activating PI3K/AKT signaling pathway.
维普
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