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Abstract

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.