Moore Amy H, Olschowka John A, O'Banion M Kerry
Department of Neurobiology and Anatomy, University of Rochester School of Medicine and Dentistry, 601 Elmwood Avenue, Box 603, Rochester, NY 14642, USA.
J Neuroimmunol. 2004 Mar;148(1-2):32-40. doi: 10.1016/j.jneuroim.2003.11.001.
Interleukin (IL)-1beta is a proinflammatory cytokine expressed in neural tissue following injury and in neurodegenerative states. To understand the consequences of its presence in brain, we carried out intraparenchymal IL-1beta injections and found significant increases in prostaglandin (PG)E2, a critical factor in inflammatory and physiological processes. Elevated mRNA and protein expression of the PGE2-synthetic-related enzymes cyclooxygenase (COX)-2 and membrane-associated PGE synthase (PGES) accompanied local PGE2 production. In addition, IL-1beta stimulated protein expression of cytosolic PGES. Finally, we showed attenuation of these IL-1beta-inductions by COX-2 inhibition, suggesting in vivo regulation of both PGE synthase isoforms in the brain.
白细胞介素(IL)-1β是一种促炎细胞因子,在损伤后的神经组织以及神经退行性状态下表达。为了了解其在脑内存在的后果,我们进行了脑实质内注射IL-1β,并发现前列腺素(PG)E2显著增加,PGE2是炎症和生理过程中的关键因子。PGE2合成相关酶环氧合酶(COX)-2和膜相关PGE合酶(PGES)的mRNA和蛋白质表达升高伴随着局部PGE2的产生。此外,IL-1β刺激了胞质PGES的蛋白质表达。最后,我们表明COX-2抑制可减弱这些IL-1β诱导作用,提示脑内两种PGE合酶亚型存在体内调节。