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作 者:林秋梅 王冬梅[1] LIN Qiu-Mei;WANG Dong-Mei(College of Life Sciences,Fujian Normal University Fujian Key Laboratory of Developmental and Neurobiology,Fuzhou 350117,China)
机构地区:[1]福建师范大学生命科学学院,福建省发育与神经生物学重点实验室,福州350117
出 处:《中国生物化学与分子生物学报》2025年第2期219-229,共11页Chinese Journal of Biochemistry and Molecular Biology
基 金:国家自然科学基金(No.81400922);福建省自然科学基金(No.2022J01636)资助。
摘 要:补体系统在识别和消除病原体、清除生理碎片、协调免疫反应以及稳态等方面发挥重要作用,作为炎症反应的一种早期预警信号,异常的补体活动是病理性疼痛发病的重要诱因。补体成分3(complement 3,C3)是病理性疼痛诱发过程中补体系统激活的重要指标。实验及临床流行病学研究发现,多种病理性疼痛中周围与中枢神经C3异常升高,通过结合特异性C3受体直接或间接通过补体信号调控神经元对神经病变的反应。C3可以通过在神经元质膜上表达的特异性补体受体直接调节神经元的生命和死亡的各个方面,也可以通过募集胶质细胞和免疫细胞经各种机制将补体信号传递给神经元间接调节,补体信号指导神经元对组织损伤、神经创伤和神经病变的反应。本文主要对C3在病理性疼痛涉及的细胞因子和信号通路的机制进行综述,探讨C3成为镇痛靶点的可能性。The complement system plays an important role in identifying and eliminating pathogens,clearing physiological debris,coordinating immune response and homeostasis,etc.As an early warning signal of inflammatory response,abnormal complement activity is an important cause of pathologic pain diseases.Complement 3(C3)is an important indicator of the activation of the complement system during pathologic pain induction.Experimental and clinical epidemiological studies have found abnormal increase of C3 in peripheral and central nerve in various types of pathologic pain,and C3 directly or indirectly regulates the response of neurons to neuropathy by binding specific C3 receptors.C3 can directly regulate various aspects of neuronal life and death through specific complement receptors expressed on the plasma membrane of neurons,and can also indirectly regulate by recruiting glial cells and immune cells through various mechanisms to transmit complement signals to neurons,which guide the response of neurons to tissue injury,neurotrauma,and neuropathy.This article mainly reviews the mechanism of cytokines and signaling pathways involved in C3 in pathologic pain,and discusses the possibility of C3 as an analgesic target in pathologic pain.
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