线粒体跨细胞转移参与电针改善术后肠麻痹的作用及机制

Postoperative ileus (POI) is one of the most common complication of postoperative intestinal motility disorders. How to effectively prevent and alleviate POI is an urgent problem to be solved clinically. Studies suggest that mitochondrial damage is closely related to the occurrence of POI; Mitochondrial transfer may be a common phenomenon, it was able to resist the aggravating nerve injury and repair damage, Our previous study found that electroacupuncture can improve intestinal motility by up-regulating CX43 expression, When intestinal motility is reduced due to intestinal neuronal damage, the number of mitochondria increases in the intercellular space and neurons. It is hypothesized that there exists mitochondrial transfer between enteric glia and neurons; The study found that the important mechanism of mitochondrial transfer is dependent on the relevant pathways CX43-mediated. In this study, mitochondrial transfer as the key point, the application of live cell imaging, molecular biology and other means, the use of living cells imaging, molecular biology and other means, to investigate the effect of electroacupuncture on mitochondrial transfer through upregulation of CX43 from whole cell and tissue level, it improves the occurrence and development mechanism of POI, provides a new theoretical basis for the effect of electroacupuncture on intestinal motility, and provides a new method for preventing postoperative ileus.

术后肠麻痹（postoperative ileus，POI）为术后肠道动力障碍相关疾病，是术后最常见的并发症之一，有效预防和减轻POI是临床急需解决的难题。研究认为线粒体损伤与POI发生密切相关；线粒体跨细胞转移可能是抵抗神经损伤加剧、促进损伤修复的普遍现象，我们前期研究发现，电针能够上调CX43改善肠动力减低，当肠道神经元损伤导致肠道动力减低出现时，细胞间隙和神经元内的线粒体数量增多，由此推测线粒体跨细胞转移存在于肠神经胶质细胞与肠神经元之间；而研究发现位于缝隙连接CX43所依赖的相关途径是线粒体跨细胞转运的重要机制。本研究拟以线粒体跨细胞转移为切入点，应用活细胞成像、分子生物学等手段，从整体和组织细胞水平探讨电针通过CX43调控线粒体跨细胞转移，改善POI的发生发展机制，为电针对肠动力的作用提供新的理论依据。

术后肠麻痹（postoperative ileus，POI）是术后最常见的并发症之一，为术后肠道动力障碍相关疾病，已知针刺或电针刺激治疗胃肠道功能紊乱疗效确切，但电针（EA）对POI的疗效及其机制有待阐明。本项目采用功能、形态和分子生物学等综合方法，研究新发现位于肠神经胶质细胞(EGCs)上的大麻素受体CB1通过CX43对线粒体功能的影响在EA治疗POI的调控作用及其分子机制。我们的结果发现：EA能够显著改善POI，同时发现POI后EGCs被激活，标记物GFAP上调，EA能明显改善POI抑制GFAP上调，进而抑制EGCs上的CB1表达，引起CX43上调，进而改变线粒体的超微结构、生物发生及钙离子兴奋性，从而改善POI和炎症指标。上述结果表明：EA通过抑制EGCs的激活下调CB1，上调CX43促进线粒体超微结构修复，改善生物发生和钙离子兴奋性而改善POI，表明EA可用于POI的研究与治疗。