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机构地区:[1]中国人民解放军第二零八医院肾内科,吉林长春130062 [2]吉林大学第二医院,吉林长春130041
出 处:《贵阳医学院学报》2014年第1期70-73,共4页Journal of Guiyang Medical College
摘 要:目的:观察氟伐他汀(Flu)对糖尿病(DM)大鼠模型中肾脏p27kipl蛋白表达的影响,探讨其对糖尿病肾脏组织保护作用的机制。方法:将成年雄性Wistar大鼠随机分为4组,正常对照组(C),氟伐他汀对照组(CF),DM模型组(DM),氟伐他汀模型组(DMF);DM组和DMF组大鼠一次性腹腔注射链脲霉素(STZ)制成糖尿病大鼠模型,C组和CF组注射等量的枸橼酸-枸橼酸钠缓冲液;模型成功后CF组、DMF组即给予氟伐他汀灌胃,其余2组大鼠给予等量蒸馏水灌胃;实验8 W时检测血清中生化指标和24 h尿蛋白,并计算肌酐清除率(Ccr)和肾脏肥大指数(KHI);免疫组织化学技术及Western blot检测肾脏组织中p27kipl蛋白表达水平。结果:实验8 W后,DM组、DMF组的血甘油三酯(TG)、胆固醇(TC)、24 h尿蛋白、KHI、Ccr高于C组和CF组(P<0.05),DMF组24 h尿蛋白、KHI、Ccr低于DM组(P<0.05);免疫组织化学技术半定量分析显示,DMF组中p27kipl蛋白表达水平较DM组降低(P<0.05);Western blot免疫印迹条带显示,DM、DMF组p27kipl水平较C、CF组明显增高(P<0.01),DMF组p27kipl相对表达量低于DM组(P<0.05)。结论:氟伐他汀有非依赖降脂的肾脏保护作用,其机制之一是通过调节细胞周期激酶抑制剂p27kipl表达而实现。Objective:To study the effect of fluvastatin on p27kipl in the kidney tissue of rats with diabetes mellitus,to explore the mechanism of its protective effect on kidney tissue of rats with diabetes mellitus.Methods:Adult male Wistar rats were randomly divided into four groups,normal control group(group C),Flu-treated control group(group CF),DM model group (group DM) and Flu-treated DM group (group DMF).DM rat model was induced by STZ intraperitoneal injection.Once the models were sucessfully established,fluvastatin was given to group CF and DMF,then tested for bio-chemist index and quantity of 24 hour urinary protein,and then Ccr and KHI were calculated.The p27kipl expressions were assessed by immunohistochemistry.The p27kipl expression was detected by Western blot.Results:Semiquantitative analysis with immunohistochemistry technique showed that p27kipl expressions in group DMF were decreased compared with group DM (P 〈 0.05).Western blot showed that p27kipl expression in group DM and DMF was much higher than group C and CF(P 〈0.01),and the relative p27kipl expression of group DMF was lower than group DM(P 〈 0.05).Conclusions:The protection of fluvastatin to the kidney,through the effect of independent decreasing blood lipid,one of the effective mechanisms is adjusting the CKI p27kipl,repressing the abnormal proliferation and hypertrophy of renal cells.
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