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作 者:陈晓岚[1] 钱桐荪[1] 徐君杰[1] 蒋季杰[1]
出 处:《天津医药》1997年第3期154-157,共4页Tianjin Medical Journal
摘 要:探讨卡介苗(BCG)对家兔系膜增殖性肾炎(MsPGN)模型的保护作用及其机制。20只家兔随机分为A、B、C 3组,A、B两组均注射小牛血清白蛋白(BSA)等以建立MsPGN模型,C组为正常对照组。在静注BSA3周前A组注射BCG,B组注射生理盐水,10周实验结束。结果示:A组循环免疫复合物、肾小球细胞数、IgG沉积程度比B组明显减少(P<0.01),光镜和电镜下A组病变明显为轻,B组电子致密物较多。刀豆素-A诱导的T淋巴细胞转化试验示A组较B组增强(P<0.05),A、B两组24h尿蛋白、Scr和抗BSA抗体滴度无明显差异。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,同时能增强T细胞淋转功能。其保护机制可能是通过增强单核吞噬细胞系统吞噬功能和Ts功能实现的。This study was aimed at the protective role of BCG on the rabbit model of mesangial proliferative glomerulonephritis (MsPGN) and its mechanism. Twenty rabbits were divided into 3 groups at rap-dom. Group C(n=6)was taken as a normal control, group A and B (n=7 each)were MsPGN models, which were the modified models of chronic serum GN induced by bovine serum albumin (BSA) intravenous injection for 6 weeks. BCG was given intravenously to group A and NS to group B respectively 3 weeks prior to the injection of BSA and twice a week for the first six weeks,and then once a week for four weeks. The results showed that the CIC levels, glomerular IgG deposits and cell counts per glomerulus in group A were significantly less than those in group B,but there was no significant difference between group A and C. The corresponding pathologic findings, whether examined by LM or by EM,were much lighter in group A;group A had a higher concavalin-A(Con-A)stimulated T lymphocyte transformation (mainly to supressive T cells) than group B did. All these evidences indicated that BCG could accelerate the clearance of CIC,reduce the IC deposits in glomeruli,mitigate the pathological changes, and strengthen the Con-A stimulated T lymphocyte transformation. It is concluded that BCG could play a protective role on the rabbit model of MsPGN, which may be obtained by strengthening the activity of mononuclear phagocyte system(MPS) so as to reduce the IC deposits in glomeruli,thus inhibit the antibody synthesis.
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