摘要
疼痛做为一种慢性疾病威胁着全球数百万患者,而目前的治疗方法效果欠佳且不良反应较多。目前已证实胶质细胞的激活参与突触前/后神经元细胞间的信号传导,并促进细胞因子、化学趋化因子、前炎性因子和肿瘤坏死因子的释放和激酶通路的信号传导,最终导致神经元超兴奋性,临床上则表现为痛觉过敏或痛觉异常。因此对疼痛发病机制尤其是分子生物学机制的认识将为我们寻找新的疼痛靶向治疗方法提供希望。
Neuropathic pain is a chronic illness affecting millions of people worldwide, and current treatments are often inadequate, ineffective or accompanied with potential severe side effects. A great deal of researches in the past decade have demonstrated the activation of glial constitutes a vital signaling network between pre-synaptic neurons and post-synaptic neurons, contributing to the release of cytokines, chemtaxin, proinflammatory factors and tumor necrosis factor, facilating the kinase pathways and finally leading to the activation of neurons. Clinical manifestations include hyperalgesia and allodynia. However further identification of pain mechanism, especially its molecular mechanism will help us find the new approach for pain management.
出处
《基础医学与临床》
CSCD
北大核心
2011年第2期222-224,共3页
Basic and Clinical Medicine
