背景:腹部手术引起的肠道炎症是术后肠梗阻(POI)发展的重要因素。ST36电针(EA)已被证明可以缓解肠道炎症并恢复POI的胃肠道动力障碍。本研究旨在阐明参与POI中EA抗炎特性的神经免疫途径。
方法:进行肠道操作(IM)诱导POI后,IM后24小时评估肠道炎症和运动,通过评估胃肠道运输(GIT),细胞因子表达,和白细胞浸润。实验手术,药理干预,基因敲除小鼠用于阐明EA的神经免疫机制。
结果:在小鼠IM后,ST36处的EA显着改善了GIT并降低了促炎细胞因子的表达和肠肌层中白细胞的浸润。膈下迷走神经切断术消除了EA治疗的抗炎作用,而脾切除术并不妨碍EA治疗的抗炎益处。氯化六甲铵(HEX)的给药有助于显着降低EA抑制炎症和增强运动功能障碍的能力,EA在α7烟碱乙酰胆碱受体(α7nAChR)敲除小鼠中无效。
结论:ST36处的EA通过需要迷走神经支配但独立于脾脏的神经回路预防肠道炎症和运动障碍。进一步的发现表明,该过程涉及肠神经元介导迷走神经信号,并需要α7nAChR的存在。这些发现表明,在ST36处利用EA可能代表POI和其他免疫相关胃肠道疾病的可能治疗方法。
BACKGROUND: The induction of intestinal inflammation as a result of abdominal surgery is an essential factor in postoperative ileus (POI) development. Electroacupuncture (EA) at ST36 has been demonstrated to relieve intestinal inflammation and restore gastrointestinal dysmotility in POI. This study aims to elucidate the neuroimmune pathway involved in the anti-inflammatory properties of EA in POI.
METHODS: After intestinal manipulation (IM) was performed to induce POI, intestinal inflammation and motility were assessed 24 h post-IM, by evaluating gastrointestinal transit (GIT), cytokines expression, and leukocyte infiltration. Experimental surgery, pharmacological intervention, and genetic knockout mice were used to elucidate the neuroimmune mechanisms of EA.
RESULTS: EA at ST36 significantly improved GIT and reduced the expression of pro-inflammatory cytokines and leukocyte infiltration in the intestinal muscularis following IM in mice. The anti-inflammatory effectiveness of EA treatment was abolished by sub-diaphragmatic vagotomy, whereas splenectomy did not hinder the anti-inflammatory benefits of EA treatment. The hexamethonium chloride (HEX) administration contributes to a notable reduction in the EA capacity to suppress inflammation and enhance motility dysfunction, and EA is ineffective in α7 nicotinic acetylcholine receptor (α7nAChR) knockout mice.
CONCLUSIONS: EA at ST36 prevents intestinal inflammation and dysmotility through a neural circuit that requires vagal innervation but is independent of the spleen. Further findings revealed that the process involves enteric neurons mediating the vagal signal and requires the presence of α7nAChR. These findings suggest that utilizing EA at ST36 may represent a possible therapeutic approach for POI and other immune-related gastrointestinal diseases.