基础医学与临床 ›› 2018, Vol. 38 ›› Issue (10): 1422-1427.

• 研究论文 • 上一篇    下一篇

氯化两面针碱对糖尿病肾病模型大鼠肾脏损伤的保护作用

刘树根1,李泽玲2,罗新辉2,魏桂林2   

  1. 1. 泉州罗裳制药厂
    2. 赣南医学院第一附属医院
  • 收稿日期:2017-08-31 修回日期:2017-12-29 出版日期:2018-10-05 发布日期:2018-09-28
  • 通讯作者: 魏桂林 E-mail:3533798048@qq.com

Nitidine chloride alleviates renal injury in diabetic nephropathy rats

  • Received:2017-08-31 Revised:2017-12-29 Online:2018-10-05 Published:2018-09-28

摘要: 目的 观察氯化两面针碱对糖尿病肾病大鼠肾脏的保护作用,并探讨其可能作用机制。方法 将大鼠随机分为对照组、糖尿病肾病模型组(DN)、NC-20 和40 mg/kg干预组。在建模成功后灌胃氯化两面针碱,1次/d,一共给药7周。试剂盒检测血清中的胰岛素与胰高血糖素;过碘酸希夫(PAS)染色法观察肾脏组织病理形态学;原位末端标记法检测肾小球细胞凋亡;免疫印迹法检测肾组织中磷酸化Smad2与Smad3表达水平、TGF-β1与Smad7蛋白表达水平。结果 DN组大鼠的胰岛素含量低于对照组(P<0.05),胰高血糖素含量高于对照组(P<0.05);给予氯化两面针碱干预后,大鼠血清中的胰岛素含量增加,胰高血糖素含量下降;低剂量组肾脏的PAS染色呈弱阳性,可见弥漫性肾小球硬化,药物高剂量组无基底膜增厚及肾小管病变;肾组织中磷酸化Smad2与Smad3表达降低(P<0.05),TGF-β1与Smad7蛋白表达降低(P<0.05)。结论 氯化两面针碱对糖尿病肾病大鼠肾脏具有一定程度的保护作用,其可能是通过抑制TGF-β/Smad信号通路发挥作用。

关键词: 氯化两面针碱, 糖尿病肾病, 肾脏, TGF-β/Smad信号通路

Abstract: Objective To observe the protective effects of nitidine chloride on renal injury in diabetic nephropathy rats, and to investigate the underlying mechanisms. Methods All rats were divided into four groups: control group, diabetic nephropathy group, and diabetic nephropathy treated with nitidine chloride (20mg/kg or 40mg/kg) groups. In addition to control group, the rest of the rats were induced for diabetic nephropathy model. After the animal model was successfully established, diabetic nephropathy rats were received nitidine chloride at dose of 20mg/kg or 40mg/kg by gavage once a day, for 7 weeks. The levels of serum insulin and glucagon were determined by commercial detection kit. The pathological morphology of kidney tissues was observed by PAS staining. Cell apoptosis in glomerular was detected by TUNEL staining. The phosphorylation of Smad2 and Smad3 and the protein expression of TGF-β1 and Smad7 were analyzed by western blotting. Results After treatment with nitidine chloride, insulin level in the serum was increased, whereas the glucagon level was decreased. PAS staining showed that weak positive staining and diffuse glomerular sclerosis in low dose group. Moreover, no thickening matrix structure and renal tubular lesion could be observed in high dose group. Finally, western blotting showed that the phosphorylation of Smad2 and Smad3 and the protein expression of TGF-β1 and Smad7 in kidney tissues were significantly decreased after nitidine chloride administration.Conclusion Nitidine chloride protects against renal injury in diabetic nephropathy rats via inhibition of TGF-β/Smad signaling pathway.

Key words: nitidine chloride, diabetic nephropathy, kidney, TGF-β/Smad signaling pathway