Celastrol slows the progression of early diabetic nephropathy in rats via the PI3K/AKT pathway.
Celastrol slows the progression of early diabetic nephropathy in rats via the PI3K/AKT pathway.
复制标题
雷公藤红醇通过 PI3K/AKT 通路减缓大鼠早期糖尿病肾病的进展
DOI：
10.1186/s12906-020-03050-y
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发表时间：
2020-10-23
影响因子：
3.9
通讯作者：
Yan M
中科院分区：
文献类型：
--
作者：
Nie Y;Fu C;Zhang H;Zhang M;Xie H;Tong X;Li Y;Hou Z;Fan X;Yan M
糖尿病肾病是糖尿病最常见的微血管并发症之一，是导致终末期肾病和意外死亡的主要因素。由于雷公藤红素对肾脏系统的有益作用和微小的不良影响需要进一步阐明，因此研究了雷公藤红素在早期糖尿病肾病中的肾脏保护作用。观察高脂高糖饮食/链脲佐菌素诱导的糖尿病大鼠早期糖尿病肾病模型的ALT、AST、24 h尿蛋白定量、血尿素氮、血清肌酐含量。采用过碘酸-希夫染色、酶联免疫吸附试验、免疫组化、逆转录-聚合酶链反应、蛋白质印迹等方法，探讨雷公藤红素对糖尿病肾病大鼠肾脏的保护作用及其机制。高剂量雷公藤红素（1.5 mg/kg/d）不仅能改善糖尿病肾病（DN）大鼠的肾功能，降低血糖和24 h尿白蛋白，还能增加LC 3 II和nephrin的表达，下调PI 3 K、p-AKT的表达以及NF-κB和mTOR的mRNA水平。雷公藤红素作为一种潜在的治疗物质，通过PI 3 K/AKT通路发挥作用，以减轻糖尿病肾病的肾损伤，抑制肾小球基底膜增厚，并实现足细胞稳态。
Diabetic nephropathy serves as one of the most regular microvascular complications of diabetes mellitus and is the main factor that causes end-stage renal disease and incident mortality. As the beneficial effect and minute adverse influence of Celastrol on the renal system requires further elucidation, the renoprotective function of Celastrol in early diabetic nephropathy was investigated. In high-fat and high-glucose diet/streptozotocin-induced diabetic rats which is the early diabetic nephropathy model, ALT, AST, 24 h urinary protein, blood urea nitrogen, and serum creatinine content were observed. Periodic acid-Schiff staining, enzyme-linked immunosorbent assay, immunohistochemical analysis, reverse transcription-polymerase chain reaction, and western blot analysis were used to explore the renoprotective effect of Celastrol to diabetic nephropathy rats and the underlying mechanism. High dose of Celastrol (1.5 mg/kg/d) not only improved the kidney function of diabetic nephropathy (DN) rats, and decreased the blood glucose and 24 h urinary albumin, but also increased the expression of LC3II and nephrin, and downregulated the expression of PI3K, p-AKT, and the mRNA level of NF-κB and mTOR. Celastrol functions as a potential therapeutic substance, acting via the PI3K/AKT pathway to attenuate renal injury, inhibit glomerular basement membrane thickening, and achieve podocyte homeostasis in diabetic nephropathy.
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