[Effects of electroacupuncture on cortactin and cytoskeletal stability in lung tissue of mice with chronic obstructive pulmonary disease].

OBJECTIVES

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.

METHODS

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.

RESULTS

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).

CONCLUSIONS

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.