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出 处:《中国现代医学杂志》2013年第19期21-25,共5页China Journal of Modern Medicine
摘 要:目的观察N-乙酰半胱氨酸(NAC)对糖尿病肾脏氧化应激以及血管内皮生长因子(VEGF)、单核细胞趋化蛋白-1(MCP-1)表达的影响,探讨NAC对糖尿病肾脏的保护作用及机制。方法建立STZ糖尿病大鼠模型,随机分为正常对照组(CON组)、糖尿病模型组(DM组)和NAC低、中、高剂量(NACⅠ、NACⅡ、NACⅢ)用药组。12周后分别检测血糖、尿蛋白排泄率、肾脏质量指数、尿素及肌酐水平,测定谷胱甘肽过氧化物酶(GSH-Px)的活性;PAS染色观察肾组织形态改变;免疫组化法和Western Blot方法检测肾组织VEGF、MCP-1的蛋白表达。结果与CON组比较,DM组和NAC各剂量组尿蛋白排泄率增加(P<0.01),血清中血糖、尿素、肌酐水平升高(P<0.05),肾脏质量指数增加(P<0.01),GSH-Px活性下降(P<0.01),肾组织中VEGF、MCP-1表达水平升高(P<0.05),肾脏病理改变明显。与DM组比较,NAC各剂量组尿蛋白排泄率减少(P<0.01),血糖水平无显著差异(P>0.05),尿素、肌酐水平降低(P<0.05),肾脏质量指数下降(P<0.01),GSH-Px活性上升(P<0.05),肾组织中VEGF、MCP-1表达水平降低(P<0.05),且以高剂量组降低最明显。肾脏病理改变较轻。结论 NAC对糖尿病大鼠肾脏具有保护作用,其机制可能与抗过氧化损伤,下调VEGF、MCP-1的表达有关。【Objective】To investigate the effects of N-acetylcysteine(NAC) on VEGF,MCP-1 in diabetic kidney of rats induced with streptozocin.【Methods】Fifty male SD rats were randomly divided into normal control group,DM group and low,middle and high dose NAC groups.After 12 weeks 24 h urine protein,kidney quality index,the serum creatinine,glucose,urea,GSH-Px.Kidney tissues were collected for PAS dyeing and measured.The expressions of VEGF and MCP-1 in renal tissue were detected by immunohistochemistry SP and western blot.【Results】Compared with normal control group,the DM group and NAC dose group had 24 h urine protein increased(P〈0.01),serum glucose,urea,creatinine increased(P〈0.05),kidney quality index increased(P〈0.01),GSH-Px activity declined(P〈0.01),kidney tissue VEGF,MCP-1 express levels(P〈0.05),kidney pathological change were significant.Compared with DM group,the NAC dose group 24h urine protein reduced(P〈0.01),No significant difference in serum glucose levels(P〈0.05),urea,creatinine decreased(P〈0.05),kidney quality index reduced(P〈0.01),GSH-Px activity raised(P〈0.05),kidney tissue VEGF and MCP-1 expression level lowered(P〈0.05),kidney pathological change was lighter.【Conclusions】NAC treatment can provide renoprotection for diabetic kidney of rats effectively through reducing oxidative stress and downregulation of VEGF,MCP-1.
关 键 词:N-乙酰半胱氨酸 糖尿病肾病 氧化应激 血管内皮生长因子 单核细胞趋化蛋白-1
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