下列機制多來自動物模型（如 CLP 敗血症、缺血再灌注、DSS 結腸炎）。臨床證據支持炎症下降與腸功能改善，但屏障層級的細節仍需更多人體試驗。
Electroacupuncture (EA), particularly at Zusanli (ST36), protects the intestinal barrier in models of sepsis, inflammation, ischemia-reperfusion injury, and colitis by multiple pathways—reducing permeability, enhancing tight junctions, and modulating inflammation and immunity.
電針（尤其是足三里 ST36），在敗血症、炎症、缺血再灌注損傷及結腸炎模型中可透過多重途徑保護腸道屏障：降低通透性、增強緊密連接，並調節炎症與免疫。
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EA at ST36 activates the vagus nerve, stimulating α7 nicotinic acetylcholine receptors (α7nAChR) on macrophages and immune cells.
電針 ST36 可激活迷走神經，刺激巨噬細胞及免疫細胞上的 α7 煙鹼型乙醯膽鹼受體（α7nAChR）。
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This inhibits pro-inflammatory cytokines (TNF-α, IL-6, IL-1β, IL-8) and promotes anti-inflammatory factors (IL-10, Arg-1).
抑制促炎細胞因子（TNF-α、IL-6、IL-1β、IL-8）釋放，並促進抗炎因子（IL-10、Arg-1）。
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Reduces systemic inflammation, prevents bacterial/endotoxin translocation, and maintains intestinal barrier integrity. Vagotomy or α7nAChR blockers abolish these effects.
減輕系統性炎症，防止細菌/內毒素移位，維持腸道屏障完整性。切斷迷走神經或 α7nAChR 阻斷劑可消除此效果。
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EA upregulates tight junction proteins: ZO-1, occludin, claudins.
電針上調緊密連接蛋白：ZO-1、occludin、claudins。
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Reduces intestinal permeability (e.g., lowers serum D-lactate, FITC-dextran leakage).
降低腸道通透性（如降低血清 D-乳酸、FITC-葡聚糖洩漏）。
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Improves villus structure, reduces epithelial apoptosis, and enhances mucosal restitution.
改善絨毛結構、減少上皮細胞凋亡、促進黏膜修復。
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Increases secretory IgA (sIgA) in intestinal mucosa.
增加腸黏膜分泌型 IgA（sIgA）。
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Boosts T-cell populations (CD3+, CD4+, γ/δ T cells) and CD4+/CD8+ ratio; helps reverse immunosuppression.
提升 T 細胞亞群（CD3+、CD4+、γ/δ T 細胞）及 CD4+/CD8+ 比率，協助逆轉免疫抑制。
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Inhibits lymphocyte apoptosis via Bcl-2/Bax regulation.
透過 Bcl-2/Bax 調節抑制淋巴細胞凋亡。
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Promotes M2 macrophage polarization (anti-inflammatory phenotype).
促進 M2 巨噬細胞極化（抗炎表型）。
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Polyamines support mucosal integrity; EA enhances this in sepsis models.
多胺支持黏膜完整性；電針在敗血症模型中增強此作用。
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EA reshapes gut microbiota and upregulates cannabinoid receptor 1 (CB1).
電針重塑腸道微生物群，上調大麻素受體 1（CB1）。
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CB1 activation repairs barrier in colitis models (e.g., DSS-induced).
CB1 激活在結腸炎模型（如 DSS 誘導）中修復屏障。
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Suppresses TLR4/NF-κB signaling; reduces oxidative stress and ROS.
抑制 TLR4/NF-κB 信號，減少氧化應激與 ROS。
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Mitochondrial dynamics regulation via HO-1/PINK1 in endotoxemia.
在內毒血症中透過 HO-1/PINK1 調節線粒體動態。
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Mast cell/tryptase/PAR-2/MLCK pathway inhibition in IBS models.
在 IBS 模型中抑制肥大細胞/tryptase/PAR-2/MLCK 途徑。
These mechanisms are primarily supported by animal studies (rats/mice with CLP sepsis, ischemia-reperfusion, DSS colitis). Clinical evidence suggests reduced inflammation and improved gut function in septic patients, but translating detailed barrier-level mechanisms to humans will require more high-quality trials.
以上機制主要來自動物研究（大鼠/小鼠 CLP 敗血症、缺血再灌注、DSS 結腸炎模型）。臨床證據支持敗血症患者炎症減輕及腸功能改善，但要把「屏障層級」的細節完整轉譯到人體，仍需更多高品質研究。
Jade Health Acupuncture 
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