Elliott K R, Leonard E J
Department of Biochemistry and Molecular Biology, University of Manchester, England.
FEBS Lett. 1989 Aug 28;254(1-2):94-8. doi: 10.1016/0014-5793(89)81016-6.
Cessation of the fMLF-induced burst of human monocyte superoxide release was associated with a rise in cAMP. This was not due to inhibition of phosphodiesterase (PDE), the major form of which was the PDE IV isozyme. The action of burst inhibitors did not correlate with cAMP levels: Rolipram, a PDe IV inhibitor, increased cAMP 6-fold, with minimal effects on the burst; whereas theophylline increased cAMP less than 2-fold but decreased the burst to less than half. Although theophylline and the adenylate cyclase activator, adenosine, inhibited fMLF-induced superoxide release, they did not inhibit production of inositol phosphates. Thus, these studies on inhibition of superoxide release implicated neither cAMP nor inositol phosphates.
fMLF诱导的人类单核细胞超氧化物释放爆发的停止与cAMP的升高有关。这并非由于磷酸二酯酶(PDE)受到抑制,其主要形式是PDE IV同工酶。爆发抑制剂的作用与cAMP水平无关:PDE IV抑制剂咯利普兰使cAMP增加6倍,对爆发的影响最小;而茶碱使cAMP增加不到2倍,但使爆发减少到不到一半。尽管茶碱和腺苷酸环化酶激活剂腺苷抑制了fMLF诱导的超氧化物释放,但它们并未抑制肌醇磷酸的产生。因此,这些关于超氧化物释放抑制的研究既未涉及cAMP也未涉及肌醇磷酸。