大鼠抗Thy1系膜增生性肾小球肾炎模型发病机制探讨

Pathogenesis of Rat Mesangial Proliferative Glomerulonephritis Induced by Anti-Thy1 Antibody

目的 探讨大鼠抗 Thy1系膜增生性肾炎模型发病机制。方法 制备兔抗大鼠胸腺细胞免疫血清 (ATS) ,再将 ATS经尾静脉注射给模型组 Wistar大鼠 ,诱导其发生系膜增生性肾炎 (Ms PGN) ;另设正常对照组 ,静脉注射生理盐水。隔天测定 2 4 h尿蛋白定量 ,放免法测定血清细胞因子含量 ,显微镜观察肾脏系膜组织增殖程度 ,BI2 0 0 0图像分析系统对肾小球系膜区进行分析。分别于注射 ATS后 1、3、5及 7d各时间点处死模型组大鼠 6只。结果 模型组与对照组比较 ,尿量、饮水量变化无显著性差异 (P>0 .0 5 ) ;模型组 1、3、5及 7d尿蛋白定量与对照组相应时间点比较均明显升高 (P<0 .0 0 1～ 0 .0 0 5 ) ;各时间点大鼠血清 IL - 1、IL - 6及 TNF含量均高于对照组 (P<0 .0 0 1～ 0 .0 0 5 ) ;模型组肾小球系膜细胞及基质明显增生。结论 细胞因子可能在鼠抗

Objective To probe into the pathogenesis of rat mesangial proliferative glomerulonephritis(MsPGN) induced by anti-Thy1 antibody. Methods Anti-Thy1 serum was produced, and then intravenously injected into Wistar rats for establishing an experimental model of MsPGN. The control group received intravenous injection of normal saline. Urinary volume and urinary protein were examined every other day. The IL-1, IL-6 and TNF contents of serum were detected by radioimmunoassay. Pathologic morphology of renal section was observed with microscope and BI2000 Image Analysis System. The rats of model group were killed on the 1st, 3rd, 5th and 7th days. Results No significant difference was seen between the model group and control group in regard to the volume of urine and in-take water (P>0.05). The levels of urinary protein, IL-1, IL-6 and TNF in model group were significantly higher than those in control group at all time points (P<0.001-0.005). Glomerular mesangium cells and matrix in the model group were obviously proliferative, compared with those in control group. Conclusion It is suggested that cytokine plays an important role in the onset of MsPGN.