To investigate the function and mechanism of Alpinetin on chronic obstructive pulmonary disease (COPD) in rat model. The markers of lung injury (body weight/pulmonary function) were measured, and the protein levels of inflammatory‐, apoptosis‐, and fibrotic‐related were determined by Western blot. HE/TUNEL/Masson staining was performed to investigate the mechanisms involved. The levels of inflammatory factors lung injury were detected by ELISA. The in vivo activities of all molecules were determined using a rat model. Alpinetin suppressed the injury of alveolus pulmonis cells occurred in vivo due to the decrease in inflammatory factors and biochemical markers by reduced the expression of TGF‐β1, α‐SMA, and TNF‐α (p??.05), associated with the declined of Caspase‐3 and Caspase‐9 (p??.01). Additionally, protective affection of Alpinetin downregulated the IL‐6 and upregulated the IL‐10 (p??.01). Protective affection of Alpinetin inhibits the apoptosis, inflammation, and fibrosis of alveolus pulmonis cells in rat models.
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