Artesunate ameliorates cigarette smoke-induced airway remodelling via PPAR-γ/TGF-β1/Smad2/3 signalling pathway

Abstract Background Airway remodelling is the major pathological feature of chronic obstructive pulmonary disease (COPD), and leads to poorly reversible airway obstruction. Current pharmacological interventions are ineffective in controlling remodelling. In present study, we investigated potential role artesunate preventing treating underlying molecular mechanisms vitro vivo. Methods A COPD rat model was established by cigarette smoke (CS) exposure. After 12 weeks treatment, changes lung tissues rats were examined ELISA histochemical immunohistochemical staining. functional experiment also carried out elucidate effects artesunate. Human bronchial smooth muscle (HBSM) cells used clarify mechanisms. Results Artesunate treatment inhibited CS-induced inflammation oxidative stress a dose-dependent manner significantly reduced inhibiting α-smooth actin (α-SMA) cyclin D1 expression. PPAR-γ upregulated TGF-β1/Smad2/3 signalling inactivated vivo vitro. Furthermore, knockdown siRNA transfection abolished artesunate-mediated inhibition HBSM cell proliferation activiting pathway downregulating expression α-SMA cells. Conclusions These findings suggest that could be treat regulating PPAR-γ/TGF-β1/Smad context COPD.