[Electroacupuncture protects septic rats from acute lung injury through the JAK1/STAT3 pathway].

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 (=45) and sham operation group (=15; with laparotomy but without CLP). The rat models of sepsis were randomized into ALI group (=15) without further treatment, ALI + SEA group (=15) treated with electroacupuncture at the point far from the Zusanli acupoint for 30 min, and ALI + EA group (=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 ( < 0.01), pulmonary expressions of TNF-α and IL-6 ( < 0.01), and obvious up-regulation of JAK1, STAT3, caspase-3, and Bax expressions ( < 0.01); similar changes were also observed in ALI+SEA group ( > 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 ( < 0.01) and decreased pulmonary expressions of TNF-α, IL-6, JAK1, STAT3, caspase-3 and Bax ( < 0.01).

Conclusions: Electroacupuncture can inhibit the release of inflammatory mediators and cell apoptosis via the JAK1/STAT3 pathway to reduce lung injuries in septic rats.