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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。
Objective To observe the effects of multiglycoside of tripterycium wilfordii Hook.f. (GTW) on proteinuria and mesangial injury in experimental mesangial proliferative nephritis in vivo. Methods A rat model of reversible anti-Thy1.1 antibody nephritis (abbreviated as “anti-Thy1.1 nephritis”) was established using a monoclonal antibody (mAb) 1223. GTW intervention was used to establish a control group. The 24-hour urinary protein excretion (Upro), renal function (bloodureanitrogen, BUN), total plasma protein (TP) and glomerular morphological changes were compared, and the platelet derived growth factor (BB) was measured. PDGFBB; transforming growth factor β, TGFβ) mRNA expression levels. Results GTW inhibited Upro and mesangial membrane damage in Thy1.1 nephritis model; Anti-Thy1.1 nephritis model showed that the expression levels of proliferating factor (PDGFBB, TGFβ) mRNA in the kidney tissue were 2.84 and 1.64 times higher than those in the normal group, respectively. The overexpression of PDGFBB mRNA was down-regulated by 33.1%. Compared with the control group, the difference was significant (P<0.05). Conclusions GTW can reduce the proteinuria of mesangial proliferative nephritis model and inhibit the proliferation of mesangial cells and the deposition of extracellular matrix. These effects may be related to the down-regulation of the expression of renal proliferative factor (PDGFBB) mRNA.