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作 者:林辉[1] 吴国仲[1] 齐向明[1] 吴永贵[1]
机构地区:[1]安徽医科大学第一附属医院肾脏内科,合肥230022
出 处:《安徽医学》2005年第1期8-10,共3页Anhui Medical Journal
基 金:安徽省自然科学基金资助项目 (编号 :0 1 0 4 370 3) ;安徽省教育厅高校中青年学科带头人基金 (编号 :52 2 2 63)
摘 要:目的 探讨LY3 3 3 5 3 1对糖尿病大鼠肾组织转化生长因子 β1(TGFβ1)表达的调节作用。 方法 建立链脲佐菌素 (STZ)诱导糖尿病模型 ,随机分对照组 ,糖尿病模型组及LY3 3 3 5 3 1给药组 (10mg·kg-1·d-1,灌胃 )。 8周后应用放射活性测定法检测肾组织细胞总蛋白激酶C(PKCt)、细胞浆PKC(PKCc)及细胞膜PKC(PKCm )活性 ,免疫组化方法检测肾组织TGFβ1表达。 结果 模型组肾组织PKCt活性、PKCc活性、PKCm活性及PKCm/PKCc明显高于对照组 (P <0 .0 5 ,P <0 .0 1) ;LY3 3 3 5 3 1给药组PKCt活性、PKCc活性、PKCm活性及PKCm /PKCc明显低于模型组 (P <0 .0 5 )。模型组肾小球TGFβ1表达明显高于对照组 (P <0 .0 1) ,LY3 3 3 5 3 1对其有明显抑制作用 (P <0 .0 5 )。 结论 LY 3 3 3 5 3 1对糖尿病肾脏有明显保护作用 ,机制可能与抑制肾组织TGFβ1过度表达有关。Objective To investigate the regulation of LY333531 on the expression of transforming growth factorβ1(TGFβ1) in kidney in diabetic rats.Methods Diabetes was induced by injection of streptozotocin(STZ).Rats were randomly divided into three groups:control group,model group,LY333531(10mg·kg -1 ·d -1 ) treatment group.The protein kinase C (PKC) activities of renal tissue were measured by radioactivity after 8 weeks;the expression of TGFβ1 was observed by immunohistochemistry in glomeruli.Results The total,cytosolic and particulate fractions of PKC activity and the ratio of particulate fractions of PKC activity to total PKC activity in renal tissue were significantly lower in the LY333531 group compared with model group (P<0.05).Compared with control,glomerular expression of TGFβ1 was significantly increased in model group (P<0.01),which was significantly inhibited by LY333531 (P<0.05).Conclusion Mechanism of renoprotection of LY333531 may be,at least partly,correlated with suppression on overexpression of TGFβ1 in renal tissus of diabetic rats.
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