To explore whether electroacupuncture (EA) can increase the expression of suppressor of cytokine signaling (SOCS) 3 by affecting the expression of miR-19b-3p, inhibiting the continuous activation of janus kinase (JAK)1/signal transducer and activator of transcription (STAT) 3 signaling pathway, and improve pulmonary inflammation in chronic obstructive pulmonary disease (COPD) mice.

Forty mice were randomly divided into normal, COPD model, COPD+EA, and COPD+miR-19b-3p agomir (agomir)+EA groups. The COPD model was simulated by cigarette smoke exposure for 1 h, twice a day for 3 months. After modeling, mice in the COPD+EA group and the COPD+agomir+EA group received EA stimulation of “Feishu” (BL13) and “Zusanli” (ST36) for 30 min, once every other day, for 14 days. The mice of the COPD+agomir+EA group received intranasal drops of miR-19b-3p agomir solution (50 μL) 24 h before every EA intervention. The pulmonary ventilation functions including forced vital capacity (FVC), forced expiratory volume (FEV) at the 0.05 s and 0.1 s (FEV_0.05 and FEV_0.1), FEV_0.05/FVC and FEV_0.1/FVC were detected using a pulmonary function analysis system. The pathological morphology of lung tissue was observed after H. E. staining. The contents of interleukin (IL)-6, tumor necrosis factor (TNF)-α and IL-1β in the bronchoalveolar lavage fluid were assayed using ELISA. And the expressions of SOCS3, JAK1, STAT3, phosphorylated (p)-JAK1 and p-STAT3 proteins in the lung tissue were detected using Western blot. The expressions of miR-19b-3p, JAK1, STAT3and SOCS3 mRNA were detected using real-time fluorescence quantitative PCR.

Compared with the normal group, the COPD model group had a significant decrease in the levels of FVC, FEV_0.05, FEV_0.1, FEV_0.05/FVC and FEV_0.1/FVC, and the expression levels of SOCS3 mRNA and protein (P＜0.001) and a significant increase in the contents of IL-6, TNF-α and IL-1β, and the expression levels of miR-19b-3p, JAK1 and STAT1 mRNAs, and p-JAK/JAK1 and p-STAT3/STAT3 protein expression ratio (P＜0.001). After EA intervention, the decreased and increased levels of all the indexes mentioned above were reversed in the COPD+EA group (P＜0.001, P＜0.01, P＜0.05). The effect of the EA+agomir were significantly less than EA in up-regulating the levels of FVC, FEV_0.05, FEV_0.1, FEV_0.05/FVC and FEV_0.1/FVC, and the expression levels of SOCS3 protein and in down-regulating the contents of IL-6, IL-1β, TNF-α, and expressions of JAK1 and STAT3 mRNA, and p-STAT3/STAT3(P＜0.001, P＜0.01, P＜0.05), suggesting that the effects of EA were weakened after intranasal drops of miR-19b-3p agomir. H. E. staining showed thickened alveolar wall, obvious inflammatory cell infiltration, with some ruptured alveoli fused into large vesicles in the model group, slightly dilated alveoli and small amount of inflammatory cell infiltration in the COPD+EA group, and slight alveolar fusion, slight thickening of alveolar wall, and light inflammatory cell infiltration in the COPD+agomir+EA group.

EA can inhibit the expression of miR-19b-3p, thereby up-regulating SOCS3 expression and inhibiting the overactivation of JAK1/STAT3 signaling, thus reducing lung inflammatory reaction to improve pulmonary function in mice with COPD.

To observe the effects of electroacupuncture (EA) at "Zusanli" (ST36) and "Feishu" (BL13) points on Cortactin and cytoskeletal stability of pulmonary endothelial cells in mice with chronic obstructive pulmonary disease (COPD), and to explore the mechanism by which EA alleviates inflammatory damage in COPD.

The C57BL/6 mice were randomly divided into 5 groups: normal group, model group, EA group, Cortactin small interfering RNA (si-Cortactin) group, and si-Cortactin + EA group, with 10 mice in each group. A COPD model was established through 12 weeks of cigarette exposure. Nasal instillation of Cortactin siRNA was performed 24 h before EA treatment. EA at bilateral ST36 and BL13 with each EA session lasted for 30 min, conducted once every other day for a continuous period of 2 weeks. Pulmonary function was assessed using a small animal lung function analyzer and HE staining was used to observe lung histopathology. ELISA was employed to measure the contents of tumor necrosis factor-α (TNF-α) and Caspase-3 in bronchoalveolar lavage fluid (BALF) and serum. TUNEL assay was used to detect apoptosis of pulmonary endothelial cells, and double immunofluorescence staining was performed to assess cytoskeletal stability in pulmonary endothelial cells. The expression levels of Caspase-3 and Cortactin mRNA in lung tissue were evaluated using qPCR, while Western blot was used to measure the protein expression levels of Caspase-3 and Cortactin in lung tissues.

Compared to the normal group, the model group exhibited decreases in forced vital capacity (FVC), forced expiratory volume in 0.05 s (FEV0.05), forced expiratory volume in 0.1 s (FEV0.1), FEV0.05/FVC, and FEV0.1/FVC (P<0.001). Lung tissue showed severe inflammatory infiltration, accompanied by increased contents of TNF-α and Caspase-3 in serum and BALF (P<0.001). The expression levels of Caspase-3 mRNA and protein were elevated, while Cortactin mRNA and protein levels were reduced in lung tissue (P<0.001). There was significant apoptosis of pulmonary endothelial cells and disruption of the cytoskeletal structure (P<0.001). After treatment, the EA group demonstrated marked improvement in these parameters compared to the model group (P<0.001, P<0.01, P<0.05). Following intervention with si-Cortactin, the indicators in the si-Cortactin group worsened further (P<0.01, P<0.001, P<0.05). The si-Cortactin + EA group showed improvements in these parameters relative to the si-Cortactin group (P<0.001, P<0.05, P<0.01).

EA can alleviate inflammatory pathological damage in the lung tissues of mice with COPD, potentially through up-regulating Cortactin, stabilizing the cytoskeleton of pulmonary endothelial cells, and inhibiting apoptosis.