Protective effect of apigenin on bleomycin-induced pulmonary fibrosis in mice by increments of lung antioxidant ability and PPARγ expression. (June 2016)

• Record Type: Journal Article
• Authors: Zhou, Xiang; Gao, Tian; Jiang, Xiao-Gang; Xie, Mei-Lin
• Is Part Of: Journal of functional foods. Volume 24(2016)
• Page Start: 382
• Page End: 389
• Publication Date: 2016-06
• Subjects: Apigenin -- Pulmonary fibrosis -- Oxidative stress -- Peroxisome proliferator-activated receptor γ; EMT epithelial to mesenchymal transition -- GSH-PX glutathione peroxidase -- MMP-9 matrix metalloproteinase-9 -- NF-κB nuclear factor-κB -- PPARγ peroxisome proliferator-activated receptor γ -- ROS reactive oxygen species -- SOD superoxide dismutase -- TGF-β1 transforming growth factor-β1; Functional foods -- Analysis -- Periodicals; Food -- Biotechnology -- Periodicals; Nutrition -- Periodicals; 613.2
• DOI: 10.1016/j.jff.2016.04.039
• Languages: English
• ISSNs: 1756-4646

Abstract

Highlights: 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. 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.