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

• Apigenin might inhibit the pulmonary fibrosis induced by bleomycin in mice.
• Apigenin reduced the lung NF-κB expression via the increment of antioxidant ability.
• Apigenin reduced the lung NF-κB expression via the increment of PPARγ expression.
• Apigenin also reduced the lung MMP-9 expression and subsequent TGF-β1 expression.
• These synergic effects of apigenin reduced the TGF-β/Smad pathway-mediated fibrosis.

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.