蛋白激酶A、蛋白激酶C参与蜜蜂毒诱致的疼痛与炎症的外周机制研究
发布时间：2018-11-24 08:43
【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。 周围组织炎症所引起的痛觉过敏依赖脊髓背根神经元的兴奋性增加和初级传入伤害性感受器的敏化。伤害性刺激导致的神经递质的释放能够增加细胞内Ca2+浓度,Ca2+浓度的增加又促进钙离子依赖的蛋白激酶C(protein kinase C, PKC)的激活。PKC作为一种蛋白激酶能够影响突触传递的整个顺序,包括神经递质释放、受体敏感性、长时程增强以及离子通道活性。在前列腺素诱致的大鼠炎症模型中表明,蛋白激酶A(protein kinase A, PKA)同样也参与初级传入神经元的敏化,而且还可能与脊髓水平的伤害性疼痛过程有关。 越来越多的证据表明cAMP-PKA和二脂酰甘油(diacylglycerol, DAG)-PKC途径在伤害性疼痛的传递过程中起到重要的作用。目前关
[Abstract]:Background & AIM: inflammation caused by peripheral tissue injury is accompanied by pain (persistent spontaneous pain, hyperalgesia, etc.) but also has obvious inflammation reaction of red, 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 refers to the retrograde transmission of nociceptive impulses to peripheral nerve terminals through axonal reflex (axon reflex) and / or dorsal root reflex (dorsal root reflex) during the transmission of nociceptive impulses to the spinal cord after injury, resulting in substance P (substance P,. SP and calcitonin related gene peptide (calcitonin gene-related peptide, CGRP) release, dilate peripheral blood vessels and promote inflammation. 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. Hyperalgesia induced by peripheral inflammation depends on increased excitability of spinal dorsal root neurons and sensitization of primary afferent nociceptive receptors. The release of neurotransmitters induced by nociceptive stimulation can increase intracellular Ca2 concentration, while the increase of Ca2 concentration promotes calcium-dependent protein kinase C (protein kinase C,. PKC, as a protein kinase, can affect the entire sequence of synaptic transmission, including neurotransmitter release, receptor sensitivity, long term enhancement and ion channel activity. In the rat inflammatory model induced by prostaglandin, protein kinase A (protein kinase A, PKA) is also involved in the sensitization of primary afferent neurons and may be related to nociceptive pain at the spinal cord level. There is growing evidence that cAMP-PKA and diglyceride (diacylglycerol, DAG)-PKC pathways play an important role in the transmission of nociceptive pain. Current level
【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
本文编号：2353017
[Abstract]:Background & AIM: inflammation caused by peripheral tissue injury is accompanied by pain (persistent spontaneous pain, hyperalgesia, etc.) but also has obvious inflammation reaction of red, 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 refers to the retrograde transmission of nociceptive impulses to peripheral nerve terminals through axonal reflex (axon reflex) and / or dorsal root reflex (dorsal root reflex) during the transmission of nociceptive impulses to the spinal cord after injury, resulting in substance P (substance P,. SP and calcitonin related gene peptide (calcitonin gene-related peptide, CGRP) release, dilate peripheral blood vessels and promote inflammation. 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. Hyperalgesia induced by peripheral inflammation depends on increased excitability of spinal dorsal root neurons and sensitization of primary afferent nociceptive receptors. The release of neurotransmitters induced by nociceptive stimulation can increase intracellular Ca2 concentration, while the increase of Ca2 concentration promotes calcium-dependent protein kinase C (protein kinase C,. PKC, as a protein kinase, can affect the entire sequence of synaptic transmission, including neurotransmitter release, receptor sensitivity, long term enhancement and ion channel activity. In the rat inflammatory model induced by prostaglandin, protein kinase A (protein kinase A, PKA) is also involved in the sensitization of primary afferent neurons and may be related to nociceptive pain at the spinal cord level. There is growing evidence that cAMP-PKA and diglyceride (diacylglycerol, DAG)-PKC pathways play an important role in the transmission of nociceptive pain. Current level
【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
【共引文献】
相关博士学位论文 前2条
1 袁维秀;氯胺酮治疗慢性神经源性疼痛作用机制的实验研究[D];中国人民解放军军医进修学院;2004年
2 李连涛;潜在激痛点高敏感性的机制研究[D];山东大学;2008年
相关硕士学位论文 前3条
1 戴飞红;rSNSR1和5-HT_（2A）受体调节伤害性感受的细胞学基础[D];福建师范大学;2010年
2 吴乐;腺苷抑制大鼠脊髓背角浅层神经元的GABA反应[D];中国人民解放军第四军医大学;2003年
3 蔡巧燕;外周组织5-羟色胺2A受体在角叉菜胶诱发的炎性痛维持过程中的作用机制[D];福建师范大学;2008年
，本文编号：2353017
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