Abstract: Objective To explore the protective effect of electroacupuncture against acute lung injury (ALI) in septic rats and explore the mechanism. Methods Sixty male SD rats were randomly divided into cecal ligation and puncture (CLP)-induced sepsis group (n=45) and sham operation group (n=15; with laparotomy but without CLP). The rat models of sepsis were randomized into ALI group (n=15) without further treatment, ALI+SEA group (n=15) treated with electroacupuncture at the point far from the Zusanli acupoint for 30 min, and ALI+EA group (n=15) with electroacupuncture at Zusanli with identical frequency, intensity and duration of electrical stimulation. All the rats were sacrificed at 12 h after CLP for measurement of the weight and the wet/dry weight (W/D) ratio of the lungs. Pathological changes of the lung tissues were examined using HE staining, and the contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the homogenate of the lung tissues were detected using enzyme-linked immunosorbent assay (ELISA). TUNEL staining was used to detect the apoptotic cells, and the expressions of Bax, caspase-3 and the important proteins in the JAK1/STAT3 signaling pathway (JAK1 and STAT3) were detected with Western blotting. Results Compared with those in the sham operation group, the rats in ALI group showed obvious lung pathologies with significantly increased lung W/D ratio (P<0.01), pulmonary expressions of TNF-α and IL-6 (P<0.01), and obvious up-regulation of JAK1, STAT3, caspase-3, and Bax expressions (P<0.01); similar changes were also observed in ALI+SEA group (P>0.05). Compared with those in ALI+SEA group, the rats in ALI+EA group showed significantly milder lung pathologies, lowered lung W/D ratio (P<0.01) and decreased pulmonary expressions of TNF-α, IL-6, JAK1, STAT3, caspase-3 and Bax (P<0.01). Conclusion Electroacupuncture can inhibit the release of inflammatory mediators and cell apoptosis via the JAK1/STAT3 pathway to reduce lung injuries in septic rats.

Key words: electroacupuncture, JAK1/STAT3 pathway, sepsis, acute lung injury