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作 者:陈琼[1] 李瑛[1] 刘伏友[1] 彭佑铭[1] 孙林[1] 李军[1] 凌光辉[1] 杨阳[1] 许向青[1]
机构地区:[1]中南大学湘雅二医院肾内科,中南大学肾病研究所,肾脏病与血液净化学湖南省重点实验室,湖南长沙410011
出 处:《现代生物医学进展》2010年第14期2605-2608,共4页Progress in Modern Biomedicine
基 金:国家中医药管理局中医药科学技术研究基金(06-07ZP33);国家高等学校博士学科点专项科研新教师基金(20070533062);中南大学代谢综合征研究中心基金(DY-2008-02-03)
摘 要:目的:观察去甲斑蝥素(NCTD)对链脲佐菌素(STZ)诱导的糖尿病(DM)模型大鼠肾小球纤维粘连蛋白以及钙调磷酸酶表达的影响,探讨去甲斑蝥素抗肾小球纤维化的机制。方法:10只大鼠正常饮食为正常对照组(C)组,30只大鼠给予高脂高糖饮食+链脲佐菌素(STZ)制备DM模型,随机分3组:DM模型(D)组10只,小剂量去甲斑蝥素治疗(N1)组10只,大剂量去甲斑蝥素治疗(N2)组10只,给药8周后检测血糖,血肌酐水平变化;用免疫组化法检测肾组织肾小球纤维粘连蛋白(fibronectin,FN)以及钙调磷酸酶(calcineurin,CaN)表达,分别用realtime-PCR以及western blot法检测肾组织FN以及CaNmRNA和蛋白水平的表达。结果:模型(D)组血糖,血肌酐水平上升(P<0.05),同时肾小球区FN,CaN的表达高于正常(C)组(P<0.05)。去甲斑蝥素干预(N)组与模型组比较,去甲斑蝥素组肾小球区FN,CaN表达下调(P<0.05)。大剂量组效果更显著(P<0.05)。去甲斑蝥素(N)治疗组血糖水平,肾功能较(D)组无明显变化。结论:去甲斑蝥素能减少糖尿病大鼠肾小球区FN的表达,其作用机制可能是通过使CaN的表达下调而实现。Objective:To understand the mechanism of norcantharidin (NCTD) in the prevention of glomerulus fibrosis, we observed norcantharidin (NCTD) on the expression of fibronectin and calcineurin in kidney of STZ-induced diabetic rats.Methods:Totally 40 Sprague-Dawley rats were randomly divided into 4 groups :normal control group (group C ,n=10) , DM model group (group D, n =10), treatment group with low dose NCTD(group N1 ,n=10) , treatment group with high dose NCTD( group N2, n=10).At the 8 th weeks, the levels of serum creatinine (Scr) , blood glucose (BS)and body weight were measured .The expressions of FN and CaN in the glomerulus were examind by immunohistochemical techniques.The protein and mRNA leval changes of FN and CaN in the renal cortex were detected by realtime-PCR and western blotting.Results:At the 8 th weeks after the models were set up, compared t o group C, the levels of BS, Scr and body weight in group D showed significant differences (P0.05) .At the 8 th week, compared to group C, the expressions of FN and CaN was significantly increased in group D (P0.05).Compared t o group D, NCTD can reduce the expressions of FN and CaN (P0.05) .0101).Conclusion:Norcantharidin decreased the expression of FN in glomerulus of STZ-induced diabetic rats possibly by way of down-regulation of calcineurin.
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