首页> 中文期刊>中国糖尿病杂志 >阿托伐他汀钙对糖尿病大鼠肾脏肿瘤坏死因子α、过氧化物酶体激增剂激活受体γ及核因子κB表达影响的研究

阿托伐他汀钙对糖尿病大鼠肾脏肿瘤坏死因子α、过氧化物酶体激增剂激活受体γ及核因子κB表达影响的研究

     

摘要

目的 观察糖尿病大鼠应用阿托伐他汀钙治疗后肾脏组织TNF-α、PPAR-γ、核因子κB(NF-κB)表达情况及其对肾脏的影响. 方法 55只3月龄SD雄性大鼠随机选取10只作为正常对照(NC)组,余45只制备糖尿病大鼠模型.共40只符合造模标准,随机分为糖尿病未治疗(D)组、胰岛素治疗(Ⅰ)组、阿托伐他汀钙治疗(A)组及胰岛素联合阿托伐他汀钙治疗(Ⅰ+A)组,每组各10只.实验第4天,Ⅰ、Ⅰ+A组接受中效胰岛素治疗,A、Ⅰ+A组予阿托伐他汀钙灌胃.14周时检测TNF-α、PPAR-γ及NF-κB表达情况. 结果 糖尿病大鼠造模成功率为88.8%.糖尿病大鼠肾小球及集合管TNF-α、PPAR-γ及NF-KB表达均较NC组增高.治疗14周后,各治疗组TNF-α及PPAR-γ表达未见明显变化,而NF-κB在A、Ⅰ+A组肾小球及集合管中表达降低,肾脏组织病变减轻. 结论 阿托伐他汀钙可能通过抑制糖尿病大鼠肾脏组织中NF-κB表达发挥抗炎、保护肾脏的作用.%Objective To observe the expression of TNF-α,PPAR-γ and NF-κB in renal tissue after the use of atorvastatin in streptozotocin-induced diabetic rats.Methods Fifty five 3-month-old male SD rats were randomized into five groups(n=10,each).The normal control (NC) groupwas injected with physiological saline.Rats in the other four groups were administered a single injection of streptozotocin to induce diabetes.Forty rats with the modeled diabetes were randomized into diabetes without treatment (group D),with insulin treatment (group Ⅰ),atorvastatin treatment (group A),andinsulin +atorvastatin treatment (group Ⅰ+A)(n=10,each).From the fourth day of the trial,the Ⅰ group and Ⅰ+A group were treated with insulin twice a day,and the A group and Ⅰ+A group were given atorvastatin feeding once a day.All groups were fed with the same diet.At the end of 14th week,the rats were terminated and the kidneys were prepared for immunohistochemical examination of the expressions of TNF-α,PPAR-γ and NF-κB.Results The successful rate of diabetes modeling was 88.8%.The expressions of TNF-α,PPAR-γ and NF-κκB in the renal tissues of diabetic rats were higher than those in normal kidneys.After the treatment for 14 weeks,the expression of TNF-α and PPAR-γ were not significandy changed,while the expression of NF-κB in the A and (A+Ⅰ) groups was decreased,and the lesions of kidney were alleviated.Conclusion Atorvastatin functions to alleviate the inflammation to protect the kidney possibly via decreasing the NF-κB expression in the renal tissues of diabetic rats.

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