| Purpose:In this paper,we use the stasis evidence,which is always present in diabetic cardiomyopathy,as an entry point,and apply curcumin,an extract of blood-activating and stasis-transforming drug,to conduct an experimental study on the intervention effect of diabetic cardiomyopathy,to investigate the effect of curcumin and its mechanism of action,and to provide new ideas and methods for the treatment of diabetic cardiomyopathy.Material and method:In this experiment,palmitic acid was used to induce H9c2 cells,resulting in a hyperlipidemic cell model that mimics diabetic cardiomyopathy,and five different treatments were used to intervene and observe the effects of different treatments on the cells and the differences between them.The five groups were: cells in normal culture as blank group(Con),cells treated with palmitic acid as palmitic acid group(PA),cells treated with palmitic acid as well as curcumin as palmitic acid + curcumin group,cells treated with palmitic acid as well as gold nanoclusters as palmitic acid + Au group(Au),cells treated with palmitic acid as well as curcumin piggybacked on gold nanoclusters as palmitic acid + Au Cur group(Au Cur),the effect of curcumin on cardiomyocyte viability was examined by MTT method to determine the dosing concentration,the accumulation of lipid droplets in different groups of cells and their differences were observed by oil red O cell staining,ROS changes and differences between groups were observed by confocal fluorescence microscopy using fluorescent labeling,the expression of lipid transport related factors CD36 and PPARα were detected by WB and compared between groups.The expression of CD36,PPARα and apoptosis-related factors Bax and Bcl-2 were detected by WB and compared between groups,and the expression of lipid transport-related factor PPARα and the differences between groups were observed by cellular immunofluorescence.Results:1.The concentration of curcumin within 10 u M had no effect on cell viability.2.Almost no red lipid droplet accumulation was observed in the cells of Con group;palmitic acid group had obvious and large amount of red lipid droplets in the cells;curcumin group had significantly less red lipid droplets compared to palmitic acid group.3.The ROS level in the Con group was very low,and almost no fluorescence was observed under the microscope;the ROS level in the palmitic acid group was high,and obvious fluorescence expression was observed under the microscope;ROS was also observed in the cells of curcumin intervention,but there was a significant decrease compared with the palmitic acid group.4.Palmitic acid was able to increase the expression of CD36 and PPARα in cardiomyocytes;curcumin was able to alleviate this abnormal increase;curcumin reduced the abnormal elevation of these two until transport factors to a greater extent after binding to gold nanoclusters.5.Palmitic acid increased the expression level of Bax/Bcl-2 in cardiomyocytes,which implies an increased level of apoptosis;curcumin could inhibit the apoptosis caused by palmitic acid;curcumin reduced the apoptosis to a greater extent after binding to gold nanoclusters.Conclusion:1.Curcumin modulates diabetic cardiomyopathy by reducing the accumulation of lipid droplets in cells,attenuating abnormal lipid accumulation,decreasing ROS expression to reduce oxidative stress levels,and down-regulating the Bax/Bcl-2 ratio to mitigate apoptosis.2.The modulatory effect of curcumin on diabetic cardiomyopathy was associated with downregulation of the expression of two factors,CD36 and PPARα.3.After binding to gold nanoclusters,curcumin decreased CD36,PPARα expression and Bax/Bcl-2 ratio to a greater extent compared to curcumin,and reduced lipid accumulation and apoptosis to a greater extent. |