Curcumin Conjugated Gold Nanoclusters as Perspective Therapeutics for Diabetic Cardiomyopathy

Accumulation of lipids in the myocardium contributes to the development of cardiac dysfunctions and various chronic diseases, such as diabetic cardiomyopathy (DCM). Curcumin (Cur) can relieve lipid accumulation problems, but its efficiency is limited by poor water solubility and biocompatibility. Herein, gold nanoclusters (AuNCs) were used to improve the efficiency of Cur, and the conjugates Curcumin-AuNCs (AuCur) were developed. In the treatment of high-fat-induced myocardial cell damage, we found that AuCur could effectively reduce intracellular lipid accumulation, the increase of reactive oxygen species (ROS), the increase of mitochondrial division, and the increase of apoptosis compared with Cur. AuCur decreased the expression of the peroxisome proliferator-activated receptors-alpha subtype (PPAR alpha), and the therapeutic effect of AuCur was canceled when the expression of PPAR alpha was enhanced. For the above reasons, AuCur treated the toxic effect of high lipid on cardiomyocytes by regulating PPAR alpha, providing a new idea and method for the treatment of DCM.

Automated summary

The accumulation of lipids in the myocardium can lead to cardiac dysfunctions and chronic diseases such as diabetic cardiomyopathy (DCM). Curcumin, although effective in reducing lipid accumulation, has limitations due to poor water solubility and biocompatibility. Gold nanoclusters (AuNCs) were used to improve the efficiency of Cur, leading to the development of Curcumin-AuNCs (AuCur). AuCur was found to effectively reduce intracellular lipid accumulation, reactive oxygen species (ROS) levels, mitochondrial division, and apoptosis in high-fat-induced myocardial cell damage, by downregulating the expression of peroxisome proliferator-activated receptors-alpha subtype (PPAR alpha). The therapeutic effects of AuCur were hindered when the expression of PPAR alpha was enhanced, suggesting that AuCur treats the toxic effects of high lipid on cardiomyocytes by regulating PPAR alpha, offering a new approach for treating DCM.