急性束缚应激对蜜蜂毒诱致的疼痛和炎症的作用机制研究

发布时间：2018-10-19 10:10

【摘要】： 背景与目的外周组织损伤所致炎症既伴随有疼痛的产生(持续性自发痛、痛觉过敏等)同时又有明显的红、肿、热的炎症反应。从炎症反应的原因和过程来看,它可进一步分为神经源性和组织源性两种来源。神经源性炎症是指损伤后伤害性冲动在向脊髓传递的过程中,冲动又经轴索反射(axon reflex)和/或背根反射(dorsal root reflex)逆行传递到外周神经终末,导致P物质(substance P, SP)及降钙素相关基因肽(calcitonin gene related peptide, CGRP)等活性物质的释放,扩张外周血管,促进炎症的发生。组织源性炎症主要指局部损伤导致大量的炎性物质释放(如缓激肽、PGE2、5-HT、组胺及细胞激肽等),导致炎症的发生。从临床炎性痛的表现看,痛可分为持续性自发痛、热和/或机械性痛敏(原发性和继发性)。一般认为,炎性痛是外周炎症介质释放刺激外周伤害性感受器,继而进一步导致中枢神经元敏化所致[1,2]。研究已证明急性应激产生镇痛现象,也证明应激可独立引起炎症反应[3]。应激反应是机体以最有可能和最有效方式对抗伤害性刺激的一种非特异性防御反应,其对机体有利,若过度反而有害。神经、炎症及免疫三大系统密切相关。随着应激中下丘脑-垂体-肾上腺皮质(HPA)和交感-肾上腺髓质系统(SNS)的激活,组织开始准备应对威胁,通过发生炎症和抗伤害反应,机体开始应对可能的随之而来的感染、疼痛。故适度的应激反应可以保护机体。在目前的研究中,我们应用一个新的炎性痛动物模型(蜜蜂毒模
[Abstract]:Background and objective inflammation caused by peripheral tissue injury is accompanied by pain (persistent spontaneous pain, hyperalgesia, etc.) and also has obvious inflammatory reaction of redness, swelling and heat. According to the cause and process of inflammatory reaction, it can be further divided into two sources: neurogenic and tissue-derived. Neurogenic inflammation is the retrograde transmission of nociceptive impulses to peripheral nerve terminals via axonal reflex (axon reflex) and / or dorsal root reflex (dorsal root reflex) during the transmission of nociceptive impulses to the spinal cord after injury. It resulted in the release of substance P (substance P, SP) and calcitonin related gene peptide (calcitonin gene related peptide, CGRP) and the expansion of peripheral blood vessels. Tissue-derived inflammation mainly refers to the local injury leading to the release of a large number of inflammatory substances (such as bradykinin, PGE2,5-HT, histamine and cell kinin), leading to inflammation. From the clinical manifestations of inflammatory pain, pain can be divided into persistent spontaneous pain, heat and / or mechanical pain sensitivity (primary and secondary). It is generally believed that inflammatory pain is a peripheral nociceptive receptor that is stimulated by the release of peripheral inflammatory mediators, which further leads to CNS sensitization [1]. Studies have shown that acute stress produces analgesia, and that stress can independently induce inflammatory response [3]. Stress response is a kind of nonspecific defense response which can resist nociceptive stimuli in the most likely and effective way. It is beneficial to the body but harmful to the body if it is excessive. Nerve, inflammation and immune system are closely related. With the activation of (HPA) and (SNS) in the hypothalamus-pituitary-adrenal cortex and sympathetic adrenomedullary system during stress, tissues begin to prepare for threats, and through inflammation and anti-nociceptive responses, the body begins to respond to possible subsequent infections. pain Therefore, moderate stress can protect the body. In the current study, we used a new inflammatory pain animal model (bee venom model)
【学位授予单位】：大连医科大学
【学位级别】：硕士
【学位授予年份】：2006
【分类号】：R363

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