Homaidan F R, Zhao L, Chakroun I, Martin C A, Burakoff R
Department of Physiology, Faculty of Medicine, American University of Beirut, Lebanon.
Mediators Inflamm. 1999;8(4-5):189-97. doi: 10.1080/09629359990342.
Interleukin-1 (IL-1) is an inflammatory mediator that increases Cl- secretion in intestinal epithelial cells. To identify the signal transduction pathway(s) involved in IL-1's action, cells were treated with IL-1 and the levels of cyclooxygenase (COX) enzymes, prostaglandin E2 (PGE2) and phospholipase A2-activating protein (PLAP), and the activity of phospholipase A2 (PLA2) were measured. IL-1 caused concentration- and time-dependent increases in the levels of PLA2 activity, and/or in the levels of PLAP, COX-2 and PGE2. The IL-induced increase in PGE2 levels was biphasic, with the first peak due to the increase in PLAP levels, and the second peak due to the increase in COX-2 levels. This increase in PGE2 levels may provide a mechanism for acute and chronic inflammation in the intestine.
白细胞介素-1（IL-1）是一种炎症介质，可增加肠道上皮细胞中的氯离子分泌。为了确定参与IL-1作用的信号转导途径，用IL-1处理细胞，并测量环氧合酶（COX）、前列腺素E2（PGE2）和磷脂酶A2激活蛋白（PLAP）的水平以及磷脂酶A2（PLA2）的活性。IL-1导致PLA2活性水平、和/或PLAP、COX-2和PGE2水平呈浓度和时间依赖性增加。IL诱导的PGE2水平升高是双相的，第一个峰值是由于PLAP水平升高，第二个峰值是由于COX-2水平升高。PGE2水平的这种升高可能为肠道的急性和慢性炎症提供一种机制。
