论文部分内容阅读
目的:研究通痹灵(TBL)对佐剂性关节炎(AA)大鼠滑膜成纤维细胞增殖及滑膜细胞分泌白细胞介素1(IL1)、肿瘤坏死因子α(TNFα)和前列腺素E2(PGE2)的影响。方法:采用组织块培养的方法获得滑膜成纤维细胞,检测原代培养大鼠滑膜细胞培养上清对滑膜成纤维细胞增殖反应的影响,以及滑膜细胞培养上清中IL1、TNFα的活性和PGE2的含量。结果:TBL可以明显抑制AA大鼠滑膜成纤维细胞增殖(P<0001),下调AA大鼠滑膜细胞分泌IL1、TNFα和PGE2(P<001);消炎痛对滑膜成纤维细胞的增殖具有明显的刺激作用(P<0001),虽能显著抑制AA大鼠滑膜细胞分泌PGE2,但进一步上调了IL1、TNFα的产生(P<001)。结论:TBL治疗RA的机理之一可能是通过下调滑膜细胞的分泌功能,使AA大鼠滑膜成纤维细胞的过度增殖恢复正常
Objective: To study the effect of Tongbiling (TBL) on the proliferation of synovial fibroblasts and synovial cells secreting interleukin-1 (IL1) and tumor necrosis factor α (TNFα) in rats with adjuvant arthritis (AA). Effects of prostaglandin E2 (PGE2). METHODS: Synovial fibroblasts were obtained by tissue culture method. The effects of primary cultured rat synovial cell culture supernatants on the proliferation of synovial fibroblasts were measured, and IL1 in synovial cell culture supernatant was detected. TNF-α activity and PGE2 content. Results: TBL could significantly inhibit the proliferation of synovial fibroblasts in AA rats (P<0001), and down-regulate IL1, TNFα and PGE2 secreted by synoviocytes of AA rats (P<001); The proliferation of synovial fibroblasts was significantly stimulated (P<0001). Although it could significantly inhibit the secretion of PGE2 in synoviocytes of AA rats, it further upregulated the production of IL1 and TNFα (P< 001). Conclusion: One of the mechanisms of TBL in the treatment of RA may be through the down-regulation of the secretory function of synovial cells, and the excessive proliferation of synovial fibroblasts in AA rats may return to normal.