Tamm－Horsfall蛋白糖基组分的致肾炎作用  

Tubulointerstitial Nephritis Induced by Tamm-Horsfall Protein :the Role of Carbohydrates Moiety of THP

作　　者：侯凡凡[1] 叶任高[1] 何柏林[1] 李仕梅[1] 

机构地区：[1]中山医科大学肾脏研究所,广州南方医院肾病实验室

出　　处：《免疫学杂志》1994年第1期28-32,共5页Immunological Journal

基　　金：国家教委博士学科点专项科研基金

摘　　要：我们在体外试验中证实：Ｔａｍｍ－Ｈｏｒｓｆａｌｌ蛋白（ＴＨＰ）刺激人单核细胞产生肿瘤坏死因子和ＩＬ－１的作用依赖其糖基组分的完整。为了探讨糖基组分在ＴＨｐ所致肾小管间质肾炎（ＴＩＮ）发病机制中的作用。我们给Ｗｉｓｔａｒ大鼠肾内直接注射ＴＨＰ制成ＴＩＮ模型。该模型在发病第４ｄ即有明显的肾间质巨噬细胞（ＭΦ）浸润。用高碘酸氢化去除ＴＨＰ的糖基组分明显破坏了ＴＨＰ诱发ＴＩＮ的能力。注射去糖基ＴＨＰ的动物只有轻微的组织学和超微结构改变。肾间质浸润的ＭΦ数量明显减少，亦无肾小管功能障碍。由此表明：ＴＨＰ的糖基组分在其导致ＴＩＮ的发生、发展中具有关键作用。We demonstrated recently in vitro that Tamm-Horsfall protein (THP)stimulated human monocytes to produce tumor necrosis factor and inter leukin 1. and these activities were dependent upon its intact glycosylation. The present study was undertaken to evaluate the role of carbohydrate moiety of THP in the pathogenesis of TIN. Experimen-tal TIN was induced in Wistar rats by direct intrarenal inoculation of THP. Prominent infiltration of mononuclear cells was seen 4 days after the inoculation and with time. increased interstitial fibrosis could be seen microscopically. However.oxidative destruction of carbohydrates on THP with periodate destroyed the ability of THP to inbuced TIN. The animals cja;;emged wotj deg;ucpsu;ated fpr, of THP presented a profound reduction in tubulointerstitial injury. evidenced by both histologic and electron microscopic study as well as by the tubular functional parametrr. The results suggests that the car-bohydrate moiety of THP may play a criticl role in the pathogenesis of THP-induced TIN.

关 键 词：TH蛋白 间质性肾炎 碳水化合物 

分 类 号：R692.330.3[医药卫生—泌尿科学]