晚期糖基化终产物修饰的β_2-微球蛋白刺激人关节滑膜细胞分泌促炎症细胞因子  

β_2-microglobulin modified with advanced glycation end products induces production of proinflammatory cytokines in human type B synovial cells

作　　者：郭君其[1] 侯凡凡[1] 张训[1] 

机构地区：[1]第一军医大学南方医院肾内科中国人民解放军肾脏病研究所,广州510515

出　　处：《中华风湿病学杂志》2001年第5期285-288,共4页Chinese Journal of Rheumatology

基　　金：国家自然科学基金资助项目 ( 39970 341)

摘　　要：目的　旨在探讨晚期糖基化终产物 (AGEs)修饰的 β2 微球蛋白 (AGE β2 m)对人关节滑膜细胞的病理生物学作用。方法　分离、培养正常人关节B型滑膜细胞 ,与AGE β2 m共同孵育 ,用ELISA法检测培养上清液中肿瘤坏死因子 α(TNF α)和白细胞介素 1β (IL 1β)水平。 结果　AGE β2 m诱导滑膜细胞分泌TNF α和IL 1β ,诱导作用具有时间和剂量依赖规律。抗AGE受体抗体预处理滑膜细胞能明显抑制AGE β2 m引起的TNF α和IL 1β分泌。结论　AGE β2 m通过AGE受体介导的作用 ,刺激人类关节B型滑膜细胞产生TNF α和IL 1β ,这种生物学效应可能参与了透析相关性淀粉样变 (DRA)时关节局部的炎症反应和组织损伤。Objective To investigate the pathobiological effect of β 2 microglobulin modified with advanced glycation end products (AGE β 2m) on human type B synovial cells.Methods The normal human type B synovial cells (HSCs) were isolated and cultured in vitro with AGE β 2m. The levels of TNF α and IL 1β in the supernatants were measured by enzyme linked immunosorbent assay (ELISA).Results AGE β 2m,but not unmodified β 2m,stimulated HSCs to produce TNF α and IL 1β with a time and dose dependent manner.These effects were inhibited by preincubation of synovial cells with an antibody against AGE receptor (RAGE).Conclusion AGE β 2m stimulates HSCs to produce TNF α and IL 1β by a pathway mediated by RAGE.These pathobiological effects of AGE β 2m might contribute to the local inflammatory response and tissue damage seen in dialysis related amyloidosis.

关 键 词：晚期糖基化终产物 β2微球蛋白 关节滑膜 肿瘤坏死因子α 白细胞介素1 透析相关性淀粉样变 DRA 

分 类 号：R459.5[医药卫生—治疗学]