熊果酸对糖尿病小鼠肾病的保护作用及机制研究  

Study on the protective effect of ursolic acid on alloxan-induced diabetic renal injury and its underlying mechanisms

作　　者：齐敏友[1] 杨钧杰[1] 周斌[1] 潘定一[1] 孙娴[1] 

机构地区：[1]浙江工业大学药学院,杭州310014

出　　处：《中国应用生理学杂志》2014年第5期445-448,共4页Chinese Journal of Applied Physiology

基　　金：浙江省教育厅科研重点项目(Z201121669)

摘　　要：目的:观察熊果酸(UA)对四氧嘧啶诱导的糖尿病小鼠肾病的影响,并探讨其作用机制。方法:昆明种小鼠一次性尾静脉注射四氧嘧啶(70 mg/kg),72 h后将血糖高于13.9 mmol/L者视为糖尿病模型。随机分为对照组、模型组和UA组(35 mg/kg,i.g.),连续给药8周。测定血糖,肾脏脏器系数,肾组织中超氧化物歧化酶(SOD),丙二醛(MDA),肿瘤坏死因子-α(TNF-α)及白细胞介素-6(IL-6);HE染色观察肾组织病理变化。结果:模型组血糖、脏器指数升高;肾组织中SOD活力降低,MDA含量明显升高;TNF-α,IL-6表达增多;病理学显示模型组肾脏细胞萎缩,排列不整齐,可见炎症细胞浸润和间质增生,UA组明显改善上述变化。结论:熊果酸对四氧嘧啶致糖尿病小鼠肾脏损伤有明显的改善作用,其机制可能与降血糖,抗氧化作用和抑制炎症因子TNF-α、IL-6有关。Objective： To investigate the effect of ursolic acid （UA） on the alloxan-induced kidney injury in diabetic mice and explored its possible mechanisms. Methods： Diabetes mellitus was induced in male Kunming mice by an injection of alloxan （70 mg/kg, i.v. ）. After 72 hours, blood glucose levels were detected and mice with blood glucose levels over 13.9 mmol/L were considered as diabetic and selected for further experiment. Thirty mice were randomly divided into three groups： control, diabetic and diabetic ＋ U A（35 mg/kg/d, i.g. continuously for 8 weeks）. Blood glucose concentration, organ coefficient of kidney, blood urea nitrogen （BUN）, creatinine （Cr） as well as renal tissue levels of superoxide dismutase （SOD）, methane dicarboxylic aldehyde （MDA）, tumor necrosis factor-α （TNF-α） and interleukin-6 （IL-6） were determined. Pathology of the renal tissue was measured by hematoxylin-eesin staining. Results： Compared to the control group, blood glucose, organ coefficient of kidney, BUN and Cr increased significantly. In addition, SOD activities was reduced markedly and levels of MDA and inflammatory factors （TNF-α, IL-6） increased significantly. Renal cells from model group rats showed atrophy and disordered after HE staining and infiltration of inflammatory cells also appeared in renal tissue of the model group. These changes were significantly attenuated in the diabetic group treated with UA. Conclusion： UA can significantly reheve renal damage in mice with diabetic nephropathy induced by allox- an, which might be related to decreased blood glucose level, antioxidation effect and inhibiting the production of inflammatory factors such as TNF-α and IL-6.

关 键 词：熊果酸 糖尿病心肌病 氧化应激 肿瘤坏死因子-α 白细胞介素-6 

分 类 号：R285.5[医药卫生—中药学]