雷公藤多甙对实验性系膜增殖性肾炎蛋白尿及系膜损伤的影响

Preventive Effect of Multi-glycoside of Tripterygium Wilfordii Hook. f. on Proteinuria and Mesangial Injury in Experimental Mesangial Proliferative Glomerulonephritis

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中文关键词: 雷公藤多甙抗Thy1.1抗体肾炎细胞因子

英文关键词:Multi-glycoside of Tripterygium Wilfordii Hook. f. anti-Thy1.1 antibody glomerulonephritis cytokine

基金项目:卫生部笹川医学奖学金资助研究课题(第26期);江苏省中医药局科研项目(No.Z054)

作者	单位
万毅刚	南京大学医学院附属鼓楼医院中医科日本新泻大学研究生院肾脏分子生物学研究所
孙伟	江苏省中医院肾科
甄彦君	南京大学医学院附属鼓楼医院中医科
铃木浩一	日本新泻大学研究生院肾脏分子生物学研究所
唐泽环	日本新泻大学研究生院肾脏分子生物学研究所
河内裕	日本新泻大学研究生院肾脏分子生物学研究所
清水不二雄	日本新泻大学研究生院肾脏分子生物学研究所

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中文摘要:

目的观察雷公藤多甙(multiglycosideoftripterygiumwilfordiiHook.f.,GTW)在体内对实验性系膜增殖性肾炎蛋白尿及系膜损伤的影响。方法运用单克隆抗体(monoclonalantibody,mAb)1223建立大鼠可逆性抗Thy1.1抗体肾炎(简称“抗Thy1.1肾炎”)模型,以GTW干预,并设立对照组。比较24h尿蛋白排泄量(urinaryproteinexcretion,Upro)、肾功能(serumcreatinine,SCr;bloodureanitrogen,BUN)、血浆总蛋白(totalplasmaprotein,TP)以及肾小球形态学变化,并检测肾组织中增殖因子(plateletderivedgrowthfactorBB,PDGFBB;transforminggrowthfactorβ,TGFβ)mRNA表达水平。结果GTW抑制抗Thy1.1肾炎模型Upro和系膜损伤;抗Thy1.1肾炎模型肾组织中增殖因子(PDGFBB、TGFβ)mRNA表达水平与正常组比较,分别为其2.84倍与1.64倍,GTW使PDGFBBmRNA过高表达水平下调33.1%,与对照组比较,差异有显著性(P<0.05)。结论GTW可减少系膜增殖性肾炎模型蛋白尿,抑制系膜细胞增殖和细胞外基质沉积;这些作用可能与下调肾组织增殖因子(PDGFBB)mRNA的表达有关。

英文摘要:

ObjectiveTo observe the preventive effect of multi-glycoside of Tripterygium Wilfordii Hook. f. (GYW) on proteinuria and mesentery injury in experimental mesangial proliferative glomerulonephritis in vivo. MethodsThe reversible anti-Thy1.1 antibody glomerulo nephritis model of rats was established with monoclonal antibody 1-22-3 and intervened with GTW, and a control group was set up in the same time. Changes of 24h urinary protein excretion, serum creatinine (Scr), blood urea nitrogen (BUN), total plasma protein (TP) and glomerular morphology were observed, and the level of mRNA expression of proliferative factors, including platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-β (TGF-β), in renal tissue was determined. ResultsGTW could inhibit proteinuria and mesangial injury in anti-Thy1.1 antibody nephritis model. The PDGF-BB and TGF-β mRNA expression in the anti-Thy1.1 antibody nephritis model rats were increased for 2.84 and 1.64 times respectively to those in the normal control group. GTW could down-regulate the over-expression of PDGF-BB mRNA by 33.1%, it was significantly different to that in the control group (P<0.05). ConclusionGTW could reduce the proteinuria and inhibit mesangial cells proliferation and extracellular matrix deposition, these effects maybe related to the down-regulating of PDGF-BB mRNA expression.

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