Huang Yan, Dong Shuan, Zhang Yuan, Zhang Ye, Guo Yan, Shi Jia, Li Xiangyun, Liu Shasha, Chen Yong, Yu Jianbo
Department of Anesthesiology and Critical Care Medicine, Tianjin Nankai Hospital, Tianjin Medical University, Tianjin, China; Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital, Tianjin, China.
Department of Anesthesiology, The Heji Affiliated Hospital of Changzhi Medical College, Changzhi Medical College, Shanxi, China.
Int Immunopharmacol. 2025 Feb 6;147:113941. doi: 10.1016/j.intimp.2024.113941. Epub 2025 Jan 1.
During the process of acute lung injury (ALI) associated with sepsis, the α7nAChR in the cholinergic anti-inflammatory pathway (CAP) plays a crucial role. However, the roles of electroacupuncture (EA) and specialized pro-resolving mediators (SPMs) in this context remain unclear. In this study, we demonstrated that EA activates CAP via α7nAChR, reducing lung permeability and inflammatory cytokine release. Our results highlighted lipoxin A4 (LXA4) as a crucial SPM in this process. EA was shown to enhance LXA4 synthesis and alleviate symptoms in patients with sepsis-related acute respiratory distress syndrome (ARDS). Studies using α7nAChR-deficient mice confirmed its essential role in LXA4 regulation. Macrophages in bronchoalveolar lavage fluid (BALF) were identified as key contributors to the protective effects of LXA4, further supported by experiments involving pulmonary macrophage depletion. In summary, we discovered a novel anti-inflammatory pathway where EA activates α7nAChR, leading to increased LXA4 production and lung protection.
在脓毒症相关的急性肺损伤(ALI)过程中,胆碱能抗炎通路(CAP)中的α7烟碱型乙酰胆碱受体(α7nAChR)发挥着关键作用。然而,在此背景下,电针(EA)和特殊促解决介质(SPM)的作用仍不明确。在本研究中,我们证明EA通过α7nAChR激活CAP,降低肺通透性并减少炎性细胞因子释放。我们的结果突出了脂氧素A4(LXA4)作为这一过程中的关键SPM。研究表明,EA可增强LXA4合成并缓解脓毒症相关急性呼吸窘迫综合征(ARDS)患者的症状。使用α7nAChR基因敲除小鼠的研究证实了其在LXA4调节中的重要作用。支气管肺泡灌洗液(BALF)中的巨噬细胞被确定为LXA4保护作用的关键贡献者,涉及肺巨噬细胞耗竭的实验进一步支持了这一点。总之,我们发现了一条新的抗炎途径,即EA激活α7nAChR,导致LXA4生成增加并保护肺脏。