Bonney R J, Wightman P D, Dahlgren M E, Sadowski S J, Davies P, Jensen N, Lanza T, Humes J L
Biochem Pharmacol. 1983 Jan 15;32(2):361-6. doi: 10.1016/0006-2952(83)90568-3.
The release of the inflammatory mediators, prostaglandins (PGs), leukotrienes (LT) and lysosomal acid hydrolases (LAH), by macrophages is stimulated by endocytic stimuli such as zymosan. This process can be interfered with by specific inhibitors of phosphatidylcholine (PC) biosynthesis. The diphenylsulfone dapsone and three analogs selectively inhibited [14C]choline incorporation into PC but had varied effects on inhibition of mediator release by macrophages. Dapsone inhibited the release of PGs, LT and LAH, whereas the three closely related structural analogs inhibited LAH release only, with little or no effect on PG production.
巨噬细胞释放炎性介质,如前列腺素(PGs)、白三烯(LT)和溶酶体酸性水解酶(LAH),可由诸如酵母聚糖等内吞刺激物所激发。该过程可被磷脂酰胆碱(PC)生物合成的特异性抑制剂所干扰。二苯砜氨苯砜及三种类似物选择性抑制[14C]胆碱掺入PC,但对巨噬细胞释放介质的抑制作用各不相同。氨苯砜抑制PGs、LT和LAH的释放,而三种结构密切相关的类似物仅抑制LAH的释放,对PG生成几乎没有影响。