| Objective:To investigate the protective effect of atorvastatin on the apoptosis of H9c2 cells induced by intermittent high glucose,and whether it plays a role via the PI3K/Akt signaling pathway.Methods:The H9c2 cardiomyocytes were cultured in vitro with low glucose(5.6 mmol/L glucose).The cells with the highest growth rate in the logarithmic growth phase were randomly divided into the following 4 groups for experimental treatment and after study:1.Cardiomyocytes cultured with continuous low glucose as normal Control group;2.Volatility high glucose group:5.5mmol/L glucose and 25mmol/L glucose alternately cultured cardiomyocytes to prepare cardiomyocyte injury model;3.Volatility high glucose+atorvastatin group:Atorvastatin pre-intervention 1 Hours later,a model of cardiomyocyte injury induced by intermittent high glucose was prepared;4.groups of intermittent high glucose+Atorvastatin+LY294002;The fourth groups of methods for intervening cells were also pre-intervented with drugs for 1 hour to prepare the H9c2 cell injury model.The above groups of experimental cells were respectively examined with CCK-8 OD450μmfor cell proliferation and Annexin-V/PI double staining method for detection of apoptosis rate according to the instructions.;each group of cardiomyocyte protein was extracted,and Western blotting technique was used for PI3K/The akt signaling pathway downstream protein phosphorylation akt for semi-quantitative analysis.Results:(1)Compared with the blank control group,intermittent high glucose can increase the apoptosis of cardiomyocytes,reduce the proliferation,and decrease the phosphorylation ofAkt;(2)Compared with the intermittent high glucose groupt,the apoptosis of cardiomyocytes decreased in high-glucose+atorvastatin group,while the expression of p-Akt increased,but this effect could be reversed by the PI3K/Akt specific inhibitor LY294002.Conclusion:Intermittent high glucose have a damaging effect on cardiomyocytes.Atorvastatin may protect cardiomyocytes from apoptosis induced by fluctuating high glucose through PI3K/akt signal pathway. |