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病理性疼痛通常指由组织损伤引起的炎性痛和神经损伤引起的神经病理性痛。损伤和强烈的伤害刺激能导致痛过敏。痛过敏现象的产生是由外周敏化(初级伤害感受器的敏感性增加)和中枢敏化(脊髓背角以及其他中枢神经元敏感性增加)引起的。有些蛋白激酶通过翻译后的调节如关键膜受体和通道蛋白磷酸化而参与外周和中枢敏化的形成。特别的是多种信号通路可汇聚而激活MAPK(mitogenactivated protein kinase)。伤害性刺激、生长因子以及炎性介质均能在初级和二级痛感受神经元中激活MAPK家族成员ERK和P38。ERK和P38的激活不仅能够引起转录后过程发生改变,而且还能够通过对转录和非转录水平的调节增加多种基因的表达,从而导致损伤后痛过敏的形成和维持。
Pathological pain usually refers to the neuropathic pain caused by inflammatory pain and nerve damage caused by tissue damage. Injuries and intense irritation can cause hyperalgesia. Hyperalgesia is caused by peripheral sensitization (increased susceptibility of primary nociceptors) and central sensitization (increased spinal cord dorsal horn and other central neuronal sensitivities). Some protein kinases are involved in peripheral and central sensitization formation through posttranslational regulation such as phosphorylation of key membrane receptors and channel proteins. In particular, a variety of signaling pathways can converge and activate MAPK (mitogenactivated protein kinase). Both nociceptive stimuli, growth factors and inflammatory mediators activate MAPK family members ERK and P38 in primary and secondary pain receptors. Activation of ERK and P38 not only leads to post-transcriptional process changes, but also increases the expression of multiple genes through the regulation of transcription and non-transcriptional levels, resulting in the formation and maintenance of post-injury hyperalgesia.