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作 者:苏静[1] 吴永贵[1] 张晶晶[1] 张培[1] 任克军[1] 董婧[1] 方芳[1]
机构地区:[1]安徽医科大学第一附属医院肾内科,安徽合肥230022
出 处:《中国现代医学杂志》2009年第3期362-366,共5页China Journal of Modern Medicine
基 金:安徽省自然科学基金(No:070413100);安徽省教育厅自然科学基金(No:2006KJ316B)
摘 要:目的探讨白芍总苷(TGP)对糖尿病大鼠肾组织JAK/STAT信号通路的调节作用。方法采用链脲佐菌素(STZ)诱导大鼠糖尿病模型。随机分对照组、模型组与TGP给药组[50、100和200mg/(kg·d)],8周后应用Western杂交方法检测肾组织磷酸化JAK2(p-JAK2),磷酸化STAT3(p-STAT3)与1α(IV)型胶原表达,免疫组化方法检测肾组织转化生长因子β1(TGF-β1)表达。结果TGP给药呈剂量依赖性降低糖尿病大鼠24h尿白蛋白排泄率。Western杂交显示模型组肾组织p-JAK2、p-STAT3与1α(IV)型胶原蛋白蛋白表达显著高于对照组(P<0.01),TGP给药[50、100与200mg/(kg·d)]8周可使肾组织p-JAK2蛋白表达下降22.3%、50.5%与43.2%,p-STAT3蛋白表达下降20.9%、61.1%与42.3%,1α(IV)型胶原蛋白表达分别下降47.9%、60.4%与72.9%。模型组肾组织TGF-β1蛋白表达明显高于对照组,TGP给药组肾组织TGF-β1蛋白表达明显低于模型组(P<0.05,0.01)。结论TGP可明显改善糖尿病大鼠早期肾损害,其机制可能部分与抑制肾组织的JAK/STAT信号通路激活有关。[Objective] To investigate the effect of TGP on activation of JAK/STAT signal transduction in the kidney from diabetic rat and explore the possible renoprotection mechanisms.[Methods] Diabetes was induced with streptozotocin in rats, and TGP was orally administered once a day for 8 weeks to rats. The expression of the p-JAK2., p-STAT3 and 1α(IV) collagen protein were determined by western blot analysis and expression of TGF-β1 was measured by immunohistochemistry in the kidney. [Results] Elevated 24 hours urinary albumin excretion rate was markedly attenuated by TGP treatment. Western blot analysis and immunohistochemistry noted that the expression of p-JAK2, p-STAT3, 1α(IV) collagen protein and TGF-β1, protein in the kidney were significantly increased in diabetic rats, while they were significantly inhibited by TGP treatment. [Conclusion] Our data suggest that TGP treatment ameliorates early renal injury via the inhibition of activation of JAK/STAT signal transduction and the relevant TGF-β1-collagen IV expression in the kidney from diabetic rat.
关 键 词:糖尿病肾病 白芍总苷 信号转导 JANUS激酶 信号转导和转录活化因子
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