论文部分内容阅读
目的探讨在类风湿关节炎(RA)患者滑膜细胞中,白三烯B4(LTB4)对肿瘤坏死因子(TNF-α)和白细胞介素-1β(IL-1β)mRNA表达的作用。方法在RA患者滑膜细胞培养体系中,加入LTB4、脂多糖(LPS)、MK-886(5-脂氧化酶激动蛋白的抑制剂),采用实时定量聚合酶链反应(PCR)检测RA患者滑膜细胞中TNF-α和IL-1βmRNA表达的改变。结果原代培养的RA滑膜细胞表达基本的IL-1β和TNF-α[IL-1β/糖酵解甘油醛-3-磷酸脱氢酶(GAPDH)和TNF-α/GAPDH],分别为0.16±0.09和0.02±0.00(n=6)。加入外源性的LTB410-9～10-8mol/L后,使TNF-α和IL-1β的mRNA表达显著增高。LPS刺激内源性的LTB4增高后,也使IL-1β和TNF-αmRNA表达显著增高。在LPS存在时,MK-8861μmol/L和10μmol/L使TNF-α的mRNA表达分别下降了15%和66%(n=7,P<0.05),使IL-1βmRNA表达下降了41%和71%(n=6,P<0.01)。结论LTB4可以调节RA滑膜细胞TNF-α和IL-1βmRNA的表达。
Objective To investigate the effect of leukotriene B4 (LTB4) on the expression of tumor necrosis factor (TNF-α) and interleukin-1β (IL-1β) mRNA in synovial cells of patients with rheumatoid arthritis (RA) Methods LTB4, lipopolysaccharide (LPS) and MK-886 (inhibitor of 5-lipoxygenase-activating protein) were added to the synovial cell culture system of RA patients. Real-time quantitative polymerase chain reaction (PCR) Changes of TNF-α and IL-1β mRNA expression in membrane cells. Results Primary cultured RA synoviocytes expressed basic IL-1β and TNF-α [IL-1β / glycolytic glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and TNF-α / GAPDH] ± 0.09 and 0.02 ± 0.00 (n = 6). The addition of exogenous LTB410-9 ~ 10-8mol / L, TNF-α and IL-1β mRNA expression was significantly increased. LPS stimulation of endogenous LTB4 increased, but also make IL-1β and TNF-αmRNA expression was significantly increased. MK-8861μmol / L and 10μmol / L decreased mRNA expression of TNF-α by 15% and 66% (n = 7, P <0.05) in the presence of LPS, decreased IL-1βmRNA expression by 41% and 71% % (n = 6, P <0.01). Conclusion LTB4 can regulate the expression of TNF-α and IL-1β mRNA in RA synovial cells.