The strong perioperative stress response caused by surgical anesthesia can significantly suppress immune function, and the body is in a state of immunosuppression for 3 to 4 days after surgery, which leads to an increase in the probability of postoperative infection. Traditional Chinese medicine believes that acupuncture points can "reconcile yin and yang", promote the recovery of immune function, and help reduce the incidence of postoperative infection. Macrophages are an important type of immune cells that participate in the body's innate immunity. They have powerful phagocytosis and clearance functions. They can be polarized into M1 and M2 types under the regulation of the body, and play different roles in fighting microbial infections. Among them, the M1 type can participate in the elimination of pathogens. In this study, we will investigate the perioperative acupoint electrical stimulation to alleviate the immunosuppressive state of surgical stress mice, clarify the regulation of perioperative acupoint electrical stimulation on glucocorticoids and the relationship between NF-κB molecules and macrophage polarization.The key molecules of related pathways were verified by glucocorticoid receptor inhibitors, and it was found that electrical stimulation of acupoints during the perioperative period can affect the polarization of macrophages in surgically stressed mice to the M1 type by reducing the level of glucocorticoids and promoting the expression of NF κB molecules. Further reveal the partial mechanism of electroacupuncture regulating the anti-inflammatory and pro-inflammatory processes of macrophages in the immune response.

中文翻译：

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围手术期穴位电刺激对手术应激小鼠巨噬细胞的影响

手术麻醉引起的强烈围手术期应激反应可明显抑制免疫功能，术后3～4天机体处于免疫抑制状态，导致术后感染概率增加。中医认为，穴位可以“调和阴阳”，促进免疫功能的恢复，有助于减少术后感染的发生。巨噬细胞是参与人体先天免疫的重要免疫细胞类型。它们具有强大的吞噬和清除功能。它们在机体的调节下可极化为M1型和M2型，在对抗微生物感染方面发挥不同的作用。其中M1型可参与病原体的消灭。本研究将探讨围手术期穴位电刺激缓解手术应激小鼠的免疫抑制状态，阐明围手术期穴位电刺激对糖皮质激素的调节作用以及NF-κB分子与巨噬细胞极化的关系。相关通路的关键分子通过糖皮质激素受体抑制剂验证，发现围术期穴位电刺激可通过降低糖皮质激素水平、促进NFκB分子表达，影响手术应激小鼠巨噬细胞极化至M1型。进一步揭示电针调节免疫反应中巨噬细胞抗炎和促炎过程的部分机制。