促炎症介质对B型滑膜细胞晚期糖基化终产物受体的调节作用

EFFECTS OF PRO-INFLAMMATORY MEDIATORS ON ADVANCED GLYCATION END PRODUCT RECEPTORS IN TYPE-B SYNOVIAL CELLS

探讨促炎症介质对B型滑膜细胞晚期糖基化终产物 (AGE)受体的调节作用。通过体外实验 ,观察TNF α、IL 1β和AGE修饰的人血清白蛋白 (AGE HSA)对B型滑膜细胞AGE受体mRNA表达的影响 ,以及中和性抗TNF α和抗IL 1β抗体对AGE HSA调节作用的阻断能力。结果显示 ,滑膜B型细胞表达RAGE和AGE R3mRNA ;AGE HSA和TNF α能以时间和剂量依赖的方式下调B型滑膜细胞RAGEmRNA的表达 ,上调AGE R3mRNA的表达 ;IL 1β能以时间和剂量依赖的方式上调B型滑膜细胞AGE R3mRNA的表达 ,而对RAGEmRNA的表达无影响 ;AGE HSA对B型滑膜细胞AGE受体mRNA表达的调节作用可被抗TNF α抗体所阻断。提示促炎症介质对滑膜细胞不同的AGE受体具有不同的调节作用。

To elucidate the effects of pro inflammatory mediators on mRNA expression of AGE receptors in type B synovial cells, type B synovial cells from normal subjects were isolated and cultured in vitro with human serum albumin modified with advanced glycation end products (AGE HSA), tumor necrosis factor α(TNF α)and interleukin 1β(IL 1β). The expression of RAGE mRNA and AGE R3 mRNA was examined by RT PCR techniques. TNF α, AGE HSA and IL 1β up regulated the expression of AGE R3 mRNA in type B synovial cells in a dose and time dependent manner. In contrast, TNF α and AGE HSA down regulated the expression of RAGE mRNA in a dose and time dependent manner. IL 1β had no effect on RAGE mRNA expression. The regulatory responses induced by AGE HSA were blocked by a neutralizing polyclonal anti human TNF α antibody, suggesting that the effects of AGE HSA were mediated by TNF α. The proinflammatory mediators may regulate the gene expression of AGE receptors in type B synovial cells, and the regulatory role of these receptors is different in response to the proinflammatory mediators.