Hafström I, Ringertz B, Palmblad J, Malmsten C
Agents Actions. 1984 Dec;15(5-6):551-5. doi: 10.1007/BF01966773.
Arachidonic acid is metabolized in neutrophils by lipoxygenase to leukotrienes, which are suggested to play a central role in inflammation. The antirheumatic drug auranofin (4 micrograms/ml) was found not to inhibit neutrophil production of the lipoxygenase products 5-HETE-, 15-HETE and LTB4, in vitro when stimulated with the calcium ionophore A23187. Auranofin, however, modulated neutrophil aggregation, enzyme release and chemotaxis induced by LTB4. The results suggest that auranofin may exert some of its antirheumatic effects through affecting neutrophil responses to leukotrienes.
花生四烯酸在中性粒细胞中通过脂氧合酶代谢为白三烯,白三烯被认为在炎症中起核心作用。研究发现,抗风湿药物金诺芬(4微克/毫升)在体外受到钙离子载体A23187刺激时,并不抑制中性粒细胞产生脂氧合酶产物5-羟基二十碳四烯酸(5-HETE)、15-羟基二十碳四烯酸(15-HETE)和白三烯B4(LTB4)。然而,金诺芬可调节由LTB4诱导的中性粒细胞聚集、酶释放和趋化性。这些结果表明,金诺芬可能通过影响中性粒细胞对白三烯的反应来发挥其部分抗风湿作用。