extract alleviates ferroptosis in lung epithelial cells induced by cigarette smoke extract through miR-3,619-5p/GPX4 axis.

extract (GBE), a therapeutic drug, has anti-inflammatory and antioxidant effects that protect cells from harmful substances. Although GBE has been extensively studied in the prevention and treatment of lung diseases, its mechanism of action in chronic obstructive pulmonary disease (COPD) is unclear. In the present study, cigarette smoke extract (CSE) and cigarette smoke (CS) were used to induce COPD in cell and animal models. The expression of related genes and proteins was detected, and cell damage and lung tissue damage were evaluated via CCK-8 assays, flow cytometry analyses, ELISA, and HE staining. In HBE cells, the expression of miR-3,619-5p was upregulated after CSE induction. However, GBE treatment alleviated the impact of CSE on HBE cell damage and alleviated COPD in vivo. In addition, GBE treatment increased the expression of GPX4 by inhibiting the expression of miR-3,619-5p, and it reduced the release of the IL-6, IL-8, and TNF-α inflammatory factors. Moreover, GBE treatment decreased the production of ROS and MDA, as well as decreased the expression of the ferroptosis-related protein ACSL4, and it promoted the production of GSH and the expression of FTH1. Further, GBE treatment improved cell viability, inhibited ferroptosis, and ultimately alleviated COPD. The present findings suggest that GBE alleviates the progression of COPD through the inhibitory effect of the miR-3,619-5p/GPX4 axis on the ferroptosis process and that GBE may be an effective treatment option for COPD.