Effect of Qingying Shengmai Decoction on Activation of Akt Signaling Pathway to Protect H9c2 Cardiomy-ocytes from Hypoxia and Reoxygenation Injury
Objective:To study the protective mechanism of serum containing Qingying Shengmai Decoction on H9c2 cardiomyocyte injury induced by hypoxia and reoxygenation.Methods:In this study,H9c2 cardiomyocyte hypoxia/reoxygenation(H/R)method was used to simulate the cell model of myocardial ischemia-reperfusion injury(MIRI).The cell experiment was divided into blank serum control group,model group,low-dose drug-containing serum group,medium-dose drug-containing serum group,and high-dose drug-containing serum group.Cardiomyo-cyte activity was determined by CCK-8 method,apoptosis rate was detected by flow cytometry,SOD,LDH,MDA and CK-MB levels were detected by ELISA,and PI3K,Akt and p-Akt protein expression were detected by West-ern blotting method.Results:Compared with blank group,the cell survival rate in model group was significantly decreased,the apoptosis rate was significantly increased,the SOD level was significantly decreased,and the levels of LDH,MDA and CK-MB were significantly increased(P<0.01).Compared with model group,the survival rate was significantly increased,the apoptosis rate was significantly decreased,the SOD level was significantly in-creased,and the levels of LDH,MDA and CK-MB were significantly decreased in low,medium and high dose groups(P<0.01).Compared with control group,p-Akt protein expression level were significantly decreased(P<0.01)and p-Akt/Akt ratio were decreased in model group(P<0.05);compared with model group,intracellular p-Akt protein expression were significantly increased(P<0.01)and p-Akt/Akt ratio were increased in drug-contain-ing serum high-dose group(P<0.05).Conclusion:Serum containing Qingying Shengmai Decoction can improve the activity of hypoxic and reoxygenated cardiomyocytes,reduce the apoptosis rate,increase SOD level,decrease LDH,MDA and CK-MB levels,improve the antioxidant capacity of cells,and may reduce the damage degree of H9c2 cardiomyocytes induced by hypoxic and reoxygenation by promoting Akt phosphorylation.