青钱柳多糖对糖尿病大鼠肾脏损伤保护作用的研究

A study on protecting-role of Cyclocarya paliurus polysaccharides on the kidney injury of diabetic rats

目的:探讨青钱柳多糖对糖尿病大鼠肾脏的影响。方法:大鼠分为正常组、模型组、阳性对照组、青钱柳多糖低、中、高剂量组。正常组和模型组分别灌服生理盐水、阳性对照组给予200 mg/kg盐酸二甲双胍,青钱柳多糖低、中、高剂量组分别每天给予浓度为100 mg/kg、200 mg/kg、400 mg/kg的青钱柳多糖溶液。观察肾脏的组织病理形态学改变,测定空腹血糖(Glucose,GLU)、血肌酐(Serum Creatinine,SCr)、血尿素氮(Blood Urea Nitrogen,BUN)、24 h尿微量白蛋白(Urinary Microalbumin,UMA)和肾组织超氧化物歧化酶(Superoxide Dismutase,SOD)、过氧化氢酶(Catalase,CAT)、谷胱甘肽过氧化物酶(Glutathione Peroxidase,GSH-Px)、谷胱甘肽还原酶(Glutathione Reductase,GR)、糖基化终末产物(AGEs)及转化生长因子(TGF-β1)的水平。结果:与正常组相比,模型组大鼠肾脏损伤明显;与模型组相比,阳性对照组和青钱柳多糖各处理组肾脏损伤程度减轻。与模型组相比,青钱柳多糖高剂量组FBG、SCr、BUN和24 h UMA水平显著或极显著降低(P<0.05或P<0.01),肾组织中SOD、CAT、GSH-Px和GR水平极显著升高(P<0.01),而肾组织中AGEs水平显著降低(P<0.05),TGF-β1水平极显著降低(P<0.01)。结论:青钱柳多糖对糖尿病大鼠肾脏损伤具有保护作用,其机制可能与其降低血糖、增强肾脏抗氧化能力和减轻肾纤维化有关。

Objective:To study the effects of Cyclocarya paliurus polysaccharides on kidney of diabetic rats.Methods:Rats were divided into 6 groups,including normal group(given normal snlme),diabetic model group(given normal snlme),metformin control group(given ometformin hydrochloried),low-dose,middle-dose and high-dose of C.paliurus polysaccharides groups.Results:Compared with the normal group,the kidney injury of rats in the model group was obvious.Compared with the model group,the degree of kidney injury was reduced in the positive control group and the treatment groups of C.paliurus polysaccharides.Compared with the model group,the levels of GLU,SCr,BUN and 24 h UMA in the high-dose of C.paliurus polysaccharides group were significantly or very significantly reduced(P<0.05 or P<0.01),the levels of SOD,CAT,GSH-Px and GR in the renal tissue were very significantly increased(P<0.01),but the levels of AGEs in the renal tissue were significantly decreased(P<0.05)and the levels of TGF-β1 were very significantly decreased(P<0.01).Conclusion:The C.paliurus polysaccharides has a protective effect on renal injury in diabetic rats,and its mechanism may be related to the decrease of blood glucose,the enhancement of renal antioxidant capacity and the reduction of renal fibrosis.