文章摘要
杨志刚,张南楠.青蒿琥酯对糖尿病肾病大鼠Toll样受体及白细胞介素-8表达的影响[J].老年医学与保健,2017,23(4):283-285,289
青蒿琥酯对糖尿病肾病大鼠Toll样受体及白细胞介素-8表达的影响
Effect of Artesunate on the Expression of Toll-like Receptor and IL-8 in Diabetic Nephropathy Rats
  
DOI:10.3969/j.issn.1008-8296.2017.04.013
中文关键词: 青蒿琥酯  糖尿病肾病  类Toll受体4  白细胞介素-8
英文关键词: artesunate  diabetic nephropathy  toll-like receptor 4  interleukin-8
基金项目:
作者单位
杨志刚 福建中医药大学附属人民医院内分泌科 
张南楠 福建医科大学附属第三医院肿瘤内科 
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中文摘要:
      目的 通过检测糖尿病大鼠Toll样受体4(Toll-like receptor 4,TLR4)和白细胞介素-8(interleukin-8,IL-8)的表达,探讨青蒿琥酯保护肾脏的机制.方法 将80只雄性Wistar大鼠随机分为4组,每组20只.成功建立大鼠糖尿病肾病模型后,正常对照组与模型对照组均予1 mL/ (kg·d)生理盐水灌胃;青蒿琥酯小剂量组予10 mg/ (kg·d)青蒿琥酯灌胃;青蒿琥酯大剂量组予30 mg/ (kg·d)青蒿琥酯灌胃.给药8周后,检测大鼠24 h尿蛋白定量、血肌酐、血尿素氮、TLR4蛋白表达及IL-8表达.结果 青蒿琥酯大剂量组、青蒿琥酯小剂量组的体重高于模型对照组,肾脏肥大指数低于模型对照组,肾组织TLR4蛋白表达、血清及肾组织IL-8水平均低于模型对照组(均P<0.05).结论 青蒿琥酯能够抑制肾组织TLR4蛋白表达,减少IL-8释放,改善糖尿病肾病模型大鼠的炎症反应.
英文摘要:
      Objective To detect the expression of toll-like receptor 4 (TLR4) and interleukine-8 (IL-8) in DN rats so as to explore the protective effect of artesunate on kidney.Methods 80 Wistar rats were randomly divided into 4 groups:normal control group,model control group,high-dose artesunate group and low-dose artesunate group,20 in each;the model of diabetic nephropathy (DN) was set up in rats;1 mL saline/ (kg· d) was applied to rats in normal control group and model control group by gavage;10 mg/ (kg· d) artesunate was applied to rats in low-dose artesunate group by gavage and 30 rag/ (kg· d) to rats in high-dose artesunate group by gavage;8 weeks later,total urine protein in 24 hours,blood creatinine,urea nitrogen,and expression levels of TLR4 and IL-8 in the rats of the 4 groups were detected.Results The rat weight in high-dose and low-dose artesunate group was higher while the kidney hypertrophy index was lower than those in model control group,and the expressions of TLR4 and IL-8 were also lower than those in model control group (P<0.05).Conclusions Artesunate can effectively control the expression of renal TLR4 protein expression,decrease IL-8 expression,and improve inflammatory response of DN.
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