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

目的 观察雷公藤多甙（multi-glycoside of tripterygium wilfordii Hook．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（monoclonal antibody，mAb）1-22-3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（urinary protein excretion，Upro）、肾功能（serum creatinine，SCr；blood urea nitrogen，BUN）、血浆总蛋白（total plasma protein，TP）以及肾小球形态学变化，并检测肾组织中增殖因子（platelet-derived growth factor-BB，PDGF-BB；transforming growth factor-β，TGF-β）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（PDGF-BB、TGF-β）mRNA表达水平与正常组比较，分别为其2．84倍与1．64倍，GTW使PDGF-BB mRNA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（PDGF-BB）mRNA的表达有关。

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

OBJECTIVE: To 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. METHODS: The reversible anti-Thyl.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-beta (TGF-beta), in renal tissue was determined. RESULTS: GTW could inhibit proteinuria and mesangial injury in anti-Thyl. 1 antibody nephritis model. The PDGF-BB and TGF-beta 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). CONCLUSION: GTW 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.