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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。
In this study, human peripheral blood lymphocytes were stimulated by calcium ionophore A23187 in vitro and then detected by reverse-phase high performance liquid chromatography (LTB_4) and its stereoisomer 6-TransLTB_4. The results showed that LTB-4 and 6-TransLTB_4 produced by peripheral blood lymphocytes in patients with rheumatoid arthritis were significantly higher than those in the normal controls (P <0.001). Moreover, LTB_4 produced by peripheral blood lymphocytes in patients with active ASA was significantly higher than that in inactive ASO patients (P <0.05) .Conclusions of this study suggest that LTB_4 participates in the inflammatory process of RA and is an important inflammatory mediator, At the same time, lymphocytes can also produce LTB_4, suggesting that LTB_4 might participate in the immune pathogenesis of RA by affecting several kinds of immunocompetent cells. Our results suggest that non-steroidal anti-inflammatory drugs (NSAIDs) include not only cyclooxygenase inhibitors but also NSAIDs that are widely used today, including lipoxygenase inhibitors to reduce the production of the inflammatory mediator LTB_4, Further explore and explore.