Ginsenoside Rg1 Alleviates Podocyte Injury Induced by Hyperlipidemia via Targeting the mTOR/NF‐<i>κ</i>B/NLRP3 Axis
Tao Wang, Yanbin Gao, Rongchuan Yue, Xiaolei Wang, Yimin Shi, Jiayi Xu, Bingjie Wu, Yimeng Li
Abstract
Background . Podocyte injury plays an important role in diabetic nephropathy (DN). The aim of this study was to determine the potential therapeutic effects of the ginsenoside Rg1 on hyperlipidemia‐stressed podocytes and elucidate the underlying mechanisms. Methods . In vitro and in vivo models of DN were established as previously described, and the expression levels of relevant markers were analyzed by Western blotting, real‐time Polymerase Chain Reaction (PCR), immunofluorescence, and immunohistochemistry. Results . Ginsenoside Rg1 alleviated pyroptosis in podocytes cultured under hyperlipidemic conditions, as well as in the renal tissues of diabetic rats, and downregulated the mammalian target of rapamycin (mTOR)/NF‐ κ B pathway. In addition, Rg1 also inhibited hyperlipidemia‐induced NLRP3 inflammasome in the podocytes, which was abrogated by the mTOR activator L‐leucine (LEU). The antipyroptotic effects of Rg1 manifested as improved renal function in the DN rats. Conclusion . Ginsenoside Rg1 protects podocytes from hyperlipidemia‐induced damage by inhibiting pyroptosis through the mTOR/NF‐ κ B/NLRP3 axis, indicating a potential therapeutic function in DN.