Molecular mechanism of inflammatory pain

作     者：Yeu-Shiuan Su Wei-Hsin Sun Chih-Cheng Chen 

作者机构：Department of Life SciencesNational Central University Jhongli 32054Taiwan Institute of Biomedical Sciences Academia Sinica Taipei 115Taiwan Taiwan Mouse Clinic-National Phenotyping and Drug Testing CenterAcademia Sinica Taipei 115Taiwan 

出 版 物：《World Journal of Anesthesiology》 (世界麻醉学杂志)

年 卷 期：2014年第3卷第1期

页      面：71-81页

学科分类：10[医学] 

基　　金：Supported by(In part)Intramural Funding from Academia Sinica by grants from the National Science Council,Taiwan(NSC 102-2325-B-001-042 to Chen CC NSC 101-2321-B-008-001 to Sun WH) 

主　　题：Acid-sensing ion channel Acidosis G-protein-coupled receptor Inflammation Proton-sensing ion channel Transient receptor potential V1 

摘      要：Chronic inflammatory pain resulting from arthritis, nerve injury and tumor growth is a serious public health issue. One of the major challenges in chronic inflammatory pain research is to develop new pharmacologic treatments with long-term efficacy and few side effects. The mediators released from inflamed sites induce complex changes in peripheral and central processing by directly acting on transducer receptors located on primary sensory neurons to transmit pain signals or indirectly modulating pain signals by activating receptors coupled with G-proteins and second messengers. High local proton concentration(acidosis) is thought to be a decisive factor in inflammatory pain and other mediators such as prostaglandin, bradykinin, and serotonin enhance proton-induced pain. Proton-sensing ion channels [transient receptor potential V1(TRPV1) and the acid-sensing ion channel(ASIC) family] are major receptors for direct excitation of nociceptive sensory neurons in response to acidosis or inflammation.G-protein-coupled receptors activated by prostaglandin, bradykinin, serotonin, and proton modulate functions of TRPV1, ASICs or other ion channels, thus leading to inflammation- or acidosis-linked hyperalgesia. Although detailed mechanisms remain unsolved, clearly different types of pain or hyperalgesia could be due to complex interactions between a distinct subset of inflammatory mediator receptors expressed in a subset of nociceptors. This review describes new directions for the development of novel therapeutic treatments in pain.