论文部分内容阅读
探讨了卡介苗（ＢＣＧ）对象兔系膜增殖性肾炎（ＭｓＰＧＮ）模型的保护作用及其机理。２０只家兔随机分为Ａ，Ｂ，Ｃ三组，Ａ，Ｂ两组注射小牛血清白蛋白（ＢＳＡ）建立ＭｓＰＧＮ模地；Ｃ组作为正常对照。在静注ＢＳＡ３周前，Ａ组先注射ＢＣＧ，Ｂ组注射等渗盐水，于第１０周结束实验。结果：Ａ组循环免疫复合物、肾小球细胞数、ｌｇＧ沉积程度比Ｂ组明显减少（Ｐ＜０．０１），光镜和电镜下Ａ组的病变也明显较轻，而Ｂ组电子致密物较多。刀豆素－Ａ诱导的Ｔ淋巴细胞转化试验Ａ组较Ｂ组增强（Ｐ＜０．０５）。Ａ，Ｂ两组２４ｈ尿蛋肉、血肌酐和抗ＢＳＡ抗体滴度差异不明显。结果表明ＢＣＧ能促进ＣＩＣ清除，使ＩＣ在小球沉积减少，减轻小球系膜增殖性炎症，同时还能增强Ｔ细胞淋转功能。其保护机理可能通过增强单核巨噬细胞系统吞噬功能和抑制性Ｔ细胞（Ｔｓ）功能实现。
The protective effect and mechanism of BCG on rabbit model of mesangial proliferative glomerulonephritis (MsPGN) were explored. Twenty rabbits were randomly divided into three groups (A, B and C). A and B groups were injected with bovine serum albumin (BSA) to establish MsPGN model. C group was used as normal control. Group A was injected with BCG 3 weeks before intravenous injection of BSA. Group B was injected with isotonic saline and the experiment was finished at week 10. Results: The levels of circulating immune complex, glomerulus cells and lgG deposition in group A were significantly lower than those in group B (P <0.01). The lesions in group A under light and electron microscopy were also significantly lighter, while the group B electron density More things. Concanavalin-A-induced T lymphocyte transformation test in group A was better than that in group B (P <0.05). There was no significant difference in the titers of egg, serum creatinine and anti-BSA between groups A and B at 24 hours. The results show that BCG can promote CIC removal, IC deposition in the pellet to reduce, reduce mitochondrial proliferative inflammation, but also can enhance T lymphocyte function. Its protective mechanism may be through enhanced monocyte-macrophage system phagocytosis and suppressive T-cell (Ts) function.