摘要
内脏高敏感性是肠易激综合征(irritable bowel syndrome,IBS)特征性病理生理机制之一,其发生涉及多种肠神经分泌的递质、细胞因子和受体,内脏高敏感性的发生机制目前尚未明确,但是辣椒素受体(transient receptor potential vanilloid 1,TRPV1)上调及磷酸化介导痛觉敏化被认为是内脏高敏感性发生的关键性事件之一。PAR2-PKC通路过度活化,可介导TRPV1磷酸化,TRPV1开放阈值下降,内脏疼痛感知异常,最终导致内脏高敏感性的发生。本文就近年来关于PAR2-PKC通路调控TRPV1磷酸化及上调介导IBS内脏高敏感性的相关研究作一概述。
Visceral hyperalgesia is one of characteristic pathophysiological mechanisms of irritable bowel syndrome （ IBS） .The mechanism of visceral hyperalgesia is unclear and thought to involve a variety of enteric nervous secreted neurotransmitters , cytokines and receptors .The exact mechanism of visceral hyperalgesia at present has not yet fully un-derstood , but TRPV1 upregulation and phosphorylation mediated pain sensitization was considered to be one of the key events.Excessive activation of PAR-PKC pathway phosphorylate the TRPV 1 and lower its threshold , eventually leading to the occurring of visceral hyperalgesia .This article reviewed the recent advance about the visceral hyperalgesia led by the upregulation and phosphorylation of TRPV 1 which was regulated by PAR-PKC pathway .
出处
《胃肠病学和肝病学杂志》
CAS
2015年第4期488-490,共3页
Chinese Journal of Gastroenterology and Hepatology
基金
广西自然基金资助项目(2012GXNSFAA053099)
广西科学研究与技术开发计划基金资助项目(桂科攻1298003-7-2)
