Li Yan1, Fan Song1, Hua Li1, Yao Li2, Jie Li1, Qiao-Yan He1, Di Zhang1, Fang Wang1, Meng Zhang1, Hang Zhao1, Tian Feng1, Ying-Yong Zhao3, Si-Wang Wang4. 1. Department of Natural Medicine, School of Pharmacy, The Fourth Military Medical University, 169 Changle West Road, Xi'an, 710032, China. 2. School of Pharmacy, Shaanxi University of Chinese Medicine, Century Road, Xianyang, 712000, China. 3. Key Laboratory of Resource Biology and Biotechnology in Western China, Ministry of Education, School of Life Science, Northwest University, No. 229 Taibai North Road, Xi'an, 710069, China. Electronic address: zyy@nwu.edu.cn. 4. Department of Natural Medicine, School of Pharmacy, The Fourth Military Medical University, 169 Changle West Road, Xi'an, 710032, China. Electronic address: wangsiw@fmmu.edu.cn.
Abstract
AIMS: Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe form of idiopathic interstitial pneumonias. The pathogenesis is associated with inflammation and oxidative stress and epithelial-mesenchymal transition (EMT). Cinnamaldehyde exhibits antiinflammatory and antioxidant properties, but its effect on IPF is unknown. The present study is to investigate the anti-fibrotic effect and action mechanism of cinnamaldehyde on IPF. MATERIALS AND METHODS: IPF was induced by intratracheal bleomycin in mice. Submicron emulsion of cinnamaldehyde was given by intraperitoneal injection once everyday for 7 or 21 continuous days after bleomycin administration. Lung histological and injury indexes were analyzed. The protein expressions of inflammation and oxidative stress as well as EMT markers alpha-smooth muscle actin (α-SMA) and E-cadherin in mice and cultured A549 cells were measured. RESULTS: Cinnamaldehyde attenuated the bleomycin-induced histological injury, reduced hydroxyproline level and improved pulmonary function by the inhibiting inflammatory cytokines and reactive oxygen species production as well as enhancing total superoxide dismutase activity in bleomycin-induced mice. Cinnamaldehyde also inhibited EMT in both bleomycin-induced mice and TGF-β1-stimulated A549 cells. CONCLUSIONS: Cinnamaldehyde ameliorated bleomycin-induced IPF via inhibition of inflammation and oxidative stress and EMT.
AIMS: Idiopathic pulmonary fibrosis (IPF) is the most frequent and severe form of idiopathic interstitial pneumonias. The pathogenesis is associated with inflammation and oxidative stress and epithelial-mesenchymal transition (EMT). Cinnamaldehyde exhibits antiinflammatory and antioxidant properties, but its effect on IPF is unknown. The present study is to investigate the anti-fibrotic effect and action mechanism of cinnamaldehyde on IPF. MATERIALS AND METHODS: IPF was induced by intratracheal bleomycin in mice. Submicron emulsion of cinnamaldehyde was given by intraperitoneal injection once everyday for 7 or 21 continuous days after bleomycin administration. Lung histological and injury indexes were analyzed. The protein expressions of inflammation and oxidative stress as well as EMT markers alpha-smooth muscle actin (α-SMA) and E-cadherin in mice and cultured A549 cells were measured. RESULTS:Cinnamaldehyde attenuated the bleomycin-induced histological injury, reduced hydroxyproline level and improved pulmonary function by the inhibiting inflammatory cytokines and reactive oxygen species production as well as enhancing total superoxide dismutase activity in bleomycin-induced mice. Cinnamaldehyde also inhibited EMT in both bleomycin-induced mice and TGF-β1-stimulated A549 cells. CONCLUSIONS:Cinnamaldehyde ameliorated bleomycin-induced IPF via inhibition of inflammation and oxidative stress and EMT.