类风湿关节炎患者周围血淋巴细胞白三烯的异常与疾病关系的探讨

Abnormal proinflammatory lipoxygenase Products from Peripheral Mononuclear Cells in Patients with Rheumatoid Arthritis

本文用人类周围血淋巴细胞体外经钙离子载体 A23187刺激,然后应用反向高效液相分析法测定其生成的白三烯(LTB_4)和其立体异构体6—TransLTB_4。结果显示类风湿关节炎(RA)患者周围血淋巴细胞生成的 LTB-4和6-TransLTB_4明显高于正常对照组(P<0.001)。而且活动性类风关患者周围血淋巴细胞体外生成的 LTB_4显著高于非活动性的类风关组(P<0.05).本文的结论说明 LTB_4参于 RA 的炎症过程,是重要的炎症介质,同时说明淋巴细胞亦能生成 LTB_4,提示 LTB_4可能通过影响几种免疫活性细胞而参于 RA 的免疫发病机制。本文结论提示,非激素抗炎药物(NSAIDs)不仅包括环氧化酶抑制剂,如今广泛应用的 NSAIDs 都属于此类,还应包括脂氧化酶抑制剂以减少炎症介质 LTB_4的生成,这有待于进一步挖掘和探讨。

Mononuclear lymphocytes(MNL)isolated from peripheral blood of patients with rheumatoid arthritis(RA) were stimulated by calcium ionophone A23187.The formation of 5—lipoxygenase products leukotriene B4 (LTB4)AND 6—trans leukotriene B4(6—trans LTB4)by MNL was determinated by reverse phase high per- formence liquid chromatography(RP—HPLC).The levels of arachidonic acid metabolites via 5—lipoxygenase pathway by stimulated MNL of patients with RA were evaluated and compared with the data obtained fron a group of control subjects.Mononuclear lymphocytes from patients synthesized significantly greater amounts of LTB4,6—trans LTB4 than did cells from normal subjects(P<0.001).The products of 5—lipoxygenase of MNL from patients with active RA compared with that from patients with non—active RA,the level of LTB4 in the former group was significantly greater than that of the latter group(P<0.05).proliminary results indi- cate that LTB4 and 6—LTB4 join the inflammatory actions of RA,LTB4 is a important mediator of inflamma- tion.the results suggest LTB4 take part in immunopathology mecanism of RA through influencing several im- munoactive cells.Other suggest would show that NSAIDS includ not only cycloxygenase inhibitors but also lipoxygenase inhibitors,reducing products of inflammatory mediator LTB4.