Epimedium sagittatum Maxim ameliorates adriamycin‐induced nephropathy by restraining inflammation and apoptosis via the PI3K/AKT signaling pathway

作者：Ru Wang, Mengnan Zeng, Beibei Zhang, Qinqin Zhang, Shuangshuang Xie, Yingbo Hu, Ruyi Fan, Mengya Wang, Xiao Yu, Yuhan Zhang, Xiaoke Zheng, Weisheng Feng · 发表于：Immunity Inflammation and Disease · 年份：2023 · DOI：10.1002/iid3.904 · 被引用次数：10 · 研究领域：Renal Diseases and Glomerulopathies、Medicinal Plant Pharmacodynamics Research、Chronic Kidney Disease and Diabetes

BACKGROUND: Modern pharmacological studies show that Epimedium sagittatum Maxim (EPI) has antioxidant, antiapoptotic, anti-inflammatory effects. However, the effects of EPI on adriamycin-induced nephropathy are unclear. AIM: The main purpose of this study is to investigate the effects of EPI on adriamycin-induced nephropathy in rats. METHODS: The chemical composition of EPI was detected by high performance liquid chromatography. Network pharmacology was used to collect the effects of EPI on adriamycin nephropathy; renal histological changes, podocyte injury, inflammatory factors, oxidative stress levels, apoptosis levels, and the PI3K/AKT signaling pathway were examined. Moreover, analyze the effects of icariin (the representative component of EPI) on adriamycin-induced apoptosis and PI3K/AKT signaling pathway of NRK-52e cells. RESULTS: Network pharmacological results suggested that EPI may ameliorate adriamycin-induced nephropathy by inhibiting inflammatory response and regulating the PI3K/AKT signaling pathway. The experimental results showed that EPI could improve pathological injury, renal function, podocyte injury, and inhibit inflammation, oxidative stress, apoptosis in adriamycin-induced nephropathy rats through the PI3K/AKT signaling pathway. Furthermore, icariin inhibited adriamycin-induced mitochondrial apoptosis in NRK-52e cells. CONCLUSION: This study suggested that EPI ameliorates adriamycin-induced nephropathy by reducing inflammation and apoptosis through the P...