NMDA及其受体介导伤害性传入引起的大鼠脊髓后角环氧化酶-2表达的增加

发布时间：2018-11-14 11:15

【摘要】： 目的:前列腺素(prostaglandins, PGs),特别是前列腺素E2和前列环素是重要的炎症、疼痛和发热介质。环氧化酶(cyclooxyganese, COX)是合成PGs的限速酶,包括COX-1、COX-2和COX-3三种同工酶。COX-1称构成酶或支持酶,是机体的正常成分,在大多数组织中都有表达,通过产生前列腺素类物质以满足机体的生理需要,如对胃肠粘膜、肾功能、血管内皮细胞和血小板功能有保护作用。COX-2是诱导酶,在机体受到内、外源性伤害性刺激后产生,其诱导产生的PGs导致炎症介质的释放,诱发疼痛、炎症和免疫细胞激活等。COX-3主要存在于大脑皮层和心脏,其功能尚不清楚。在伤害性刺激传入引起痛及痛过敏时,COX-2和PGs发挥重要的作用。预先口服或鞘内给予非选择性COX抑制剂和选择性COX-2抑制剂均可产生抗伤害作用,而且选择性COX-2抑制剂能以剂量依赖的方式降低痛及痛过敏。电生理学研究表明,脊髓背侧表面给予COX抑制剂可抑制皮下注射福尔马林所诱导的脊髓后角神经元自发放电增强。免疫组织化学、Western blot等研究显示,在大鼠外周炎性痛及痛过敏模型中,脊髓中COX-2蛋白表达增加,进一步证实了COX-2与伤害性信息的传递有关。尽管持续性伤害性传入可引起脊髓COX-2表达增多,但关于其表达增多的机制目前尚不十分清楚。大量证据表
[Abstract]:Objective: prostaglandin (prostaglandins, PGs), especially prostaglandin E 2 and prostacyclin, are important mediators of inflammation, pain and fever. Cyclooxygenase (cyclooxyganese, COX) is a rate-limiting enzyme that synthesizes PGs, including three isozymes, COX-1,COX-2 and COX-3. COX-1, which forms an enzyme or a supporting enzyme, is a normal component of the body and is expressed in most tissues. By producing prostaglandins to meet the physiological needs of the body, such as the gastrointestinal mucosa, renal function, vascular endothelial cells and platelet function. COX-2 is an inducible enzyme in the body. PGs induced by exogenous nociceptive stimulation leads to the release of inflammatory mediators, pain, inflammation and immune cell activation. COX-3 exists mainly in the cerebral cortex and heart, and its function is not clear. COX-2 and PGs play an important role in pain and hyperalgesia caused by noxious stimuli afferents. Preoral or intrathecal administration of both non-selective COX inhibitors and selective COX-2 inhibitors can produce nociceptive effects, and selective COX-2 inhibitors can reduce pain and hyperalgesia in a dose-dependent manner. Electrophysiological studies showed that COX inhibitor on the dorsal side of spinal cord could inhibit the enhancement of spontaneous discharges of spinal dorsal horn neurons induced by subcutaneous injection of formalin. Immunohistochemical, Western blot and other studies showed that the expression of COX-2 protein in spinal cord was increased in rats with peripheral inflammatory pain and hyperalgesia, which further proved that COX-2 was related to the transmission of nociceptive information. Although persistent nociceptive afferents can increase the expression of COX-2 in the spinal cord, the mechanism of this increase is still unclear. Mass evidence sheet
【学位授予单位】：河北医科大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R363

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