Protective effect of apigenin on bleomycin-induced pulmonary fibrosis in mice by increments of lung antioxidant ability and PPARγ expression

Abstract

Apigenin is one of the most common flavonoids present in numerous vegetables and foods. The protective effect of apigenin on bleomycin-induced mouse pulmonary fibrosis and potential mechanisms were examined here. The results showed that after oral gavage of apigenin 150–300 mg/kg for 28 days, the lung weight coefficient, hydroxyproline content, inflammatory cells and collagen accumulation were decreased. Importantly, apigenin treatment increased the levels of lung glutathione, superoxide dismutase and peroxisome proliferator-activated receptor γ (PPARγ) expression. Moreover, apigenin simultaneously increased the levels of lung Smad-7 and E-cadherin expressions, and decreased the levels of lung nuclear factor-κB (NF-κB), transforming growth factor-β1 (TGF-β1), matrix metalloproteinase-9 and vimentin expressions. These findings demonstrate that apigenin might exert a protective effect on bleomycin-induced pulmonary fibrosis in mice, and its mechanisms were related to the increments of lung antioxidant ability and PPARγ expression, which subsequently inhibited the NF-κB/TGF-β-mediated lung epithelial to mesenchymal transition and collagen production.

Keywords

• Apigenin
• Pulmonary fibrosis
• Oxidative stress
• Peroxisome proliferator-activated receptor γ