Exploration of the effect of pterostilbene on autophagy-mediated H9C2 cardiomyocyte hypertrophy based on PI3K/Akt pathway
Objective To explore the effect of pterostilbene(PTE)on autophagy-mediated H9C2 cardiomyocyte hypertrophy based on the PI3K/Akt pathway.Methods H9C2 cardiomyocytes were cultured,and a cardiomyocyte hypertrophy model was established using 50 μ mol/L hydrogen peroxide(H2O2).Four groups were randomly divided into:the control group(Group C),the cardiomyocyte hypertrophy group(Group H),the cardiomyocyte hypertrophy+PTE group(Group H+PTE),and the cardiomyocyte hypertrophy+PTE+3-MA group(Group H+PTE+3MA).After 24 hours of intervention,Western blot was used to detect the expression of hypertrophy signaling molecule ERK and its phosphorylated protein,autophagy-related protein beclin 1 expression,and the expression of signaling pathway-related proteins PI3K and Akt and their phosphorylated protein.Results Compared with Group C,the expression of p-ERK,p-PI3K,and p-Akt in Group H increased,while the expression of beclin 1 decreased,with statistically significant differences(P<0.05).Compared with Group H,the expression of p-ERK,p-PI3K,and p-Akt in Group H+PTE decreased,while the expression of beclin1 increased,with statistically significant differences(P<0.05).Compared with Group H+PTE,the expression of p-ERK,p-PI3K,and p-Akt in Group H+PTE+3MA increased,while the expression of beclin1 decreased,with statistically significant differences(P<0.05).Conclusion PTE alleviates H202-induced H9C2 cardiomyocyte hypertrophy through enhanced autophagy,and its mechanism is related to the PI3K/Akt pathway.