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目的探讨20-羟基蜕皮甾酮(20E)对糖尿病肾病的保护作用及相关机制。方法大鼠(体重80~100 g)随机分4组,用60 mg/kg腹腔注射链脲佐菌素(STZ)造模,之后正常组和模型组、对照组和20E治疗组,分别灌服蒸馏水、5 mg/kg盐酸二甲双胍和10 mg/kg20E溶液。药物干预6周后,观察肾脏形态学改变,测定糖基化终末产物(AGEs)和转化生长因子(TGF-β1)含量,分析过氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽还原酶(GR)的表达。结果与模型组相比,20E处理后肾脏损伤程度减轻;Real-time PCR结果显示,20E处理后SOD、CAT、GSH-Px和GRmRNA水平分别增加了146.4%(P<0.05)、64.5%(P<0.05)、41.3%(P<0.05)和22.6%,同时AGEs和TGF-β1分别减少42.9%(P<0.05)和80.3%(P<0.05)。结论 20E对糖尿病肾病具有保护作用,其机制可能与诱导肾脏SOD、CAT、GSH-Px和GR表达增加及AGEs和TGF-β1含量减少有关。
Objective To investigate the protective effect of 20-hydroxy ecdysterone (20E) on diabetic nephropathy and its related mechanism. Methods Rats (weighing 80-100 g) were randomly divided into 4 groups. The rats were injected intraperitoneally with streptozotocin (STZ) at a dose of 60 mg / kg. After that, the rats in the normal group and the model group, the control group and the 20E group were dosed orally Distilled water, 5 mg / kg metformin hydrochloride and 10 mg / kg 20E solution. The changes of renal morphology were observed 6 weeks after drug intervention. The contents of AGEs and TGF-β1 were measured. The activities of superoxide dismutase (SOD), catalase (CAT) , Glutathione peroxidase (GSH-Px), glutathione reductase (GR) expression. Results The level of SOD, CAT, GSH-Px and GR mRNA in 20E treatment group increased by 146.4% (P <0.05) and 64.5% (P <0.05), 41.3% (P <0.05) and 22.6%, respectively, while AGEs and TGF-β1 decreased by 42.9% (P <0.05) and 80.3% (P <0.05), respectively. Conclusions 20E can protect diabetic nephropathy. The mechanism may be related to the increase of SOD, CAT, GSH-Px and GR expression and the decrease of AGEs and TGF-β1 in the kidney.