Baicalin Relieves Airway Inflammation in COPD by Inhibiting miR-125a

To investigate the effects of Baicalin on the apoptosis of human bronchial epithelial cells (16HBE) induced by cigarette smoke extract (CSE) and the release of inflammatory factors, and to clarify its possible mechanism. CSE was used to treat 16HBE cells and construct COPD cell model. The activity of 16HBE cells was detected by CCK-8 and BrdU. Real-time fluorescence quantitative PCR (RT-QPCR) was used to detect the expression level of miR-125a in each group of 16HBE cells. At the same time, the levels of 16HBE inflammatory cytokines IL-1β, IL-8, IL-6, and TNF-α were detected. The apoptosis rate of 16HBE cells in each group was detected by TUNEL. Compared with the control group, the proliferation of 16HBE cells in CSE group was decreased. Baicalin reversed the effect of 2% CSE on the proliferation of 16HBE cells. Baicalin also reversed the effect of 2% CSE on apoptosis and inflammatory factors in 16HBE cells. miR-125a is highly expressed in COPD, and Baicalin can inhibit the expression of miR-125a. Silencing miR-125a reduces apoptosis and inflammatory response of 16HBE cells in COPD. miR-125a reversed the effects of Baicalin on apoptosis and inflammation of 16HBE cells. Baicalin can reduce CSE-induced apoptosis of human bronchial epithelial cells and release of inflammatory factors, and its mechanism may be related to the inhibition of miR-125a.