Jiatong Hao

Pulmonary fibrosis is a chronic and aggresitive interstitial lung disease. We evaluated the anti-fibrotic effect of mogrol isolated from Siratia grosvenorii against pulmonary fibrosis and the underlying mechanism. In vitro, mogrol (10 µM) show anti-fibrotic effects by suppressing TGF-β1-induced the epithelial mesenchymal transition of alveolar epithelial cells and myofibroblasts trans-differentiation. Then, mogrol was given after intratracheal instillation of bleomycin in mice. Results showed that mogrol treatments (10 mg/kg/d) improved characteristic changes in histopathology, inflammation infiltration and collagen deposition in lung tissues, and that mogrol significantly inhibited TGF-β1-Smad2/3 pathway, restored NOX4 abnormal expression but promoted AMPK phosphorylation. Further research identified that co-treatment with AMPK inhibitor, significantly blocked the anti-fibrotic properties of mogrol, suggesting that the protective effect of mogrol may be attributed to activated AMPK with consequent reduction in inflammatory, fibrosis and oxidative stress. Overall, Siratia grosvenorii effectively protects against lung fibrosis via AMPK activation and amelioration of TGF-β1 signalling pathway.

Lipid accumulation, inflammatory responses and oxidative stress have been implicated in the pathology of alcohol-induced liver injury (ALI). In this work, we evaluated the effects of the functional food XingJiuTang (XJT) on ALI and explored the underlying mechanism. We used alcohol-stimulated human normal hepatocytes L02 for in vitro experiments, while for in vivo experiments, 55 % alcohol was intragastrically administrated to C57BL/6 mice at 16 mL/kg with pre-administration of bifendate and XJT. Liver histology and function, along with the inflammatory cytokines, oxidative mediators and SIRT1/Nrf-2 pathway were evaluated. The results showed that XJT treatment significantly alleviated ALI, ameliorated lipid peroxidation, improved the liver function impaired by alcohol and inhibited the hepatocytes apoptosis in vitro and in vivo. In addition, XJT treatment modulated the activation of the SIRT1/Nrf-2 signaling pathway and suppressed the overexpression of NOX4. Overall, the functional food XJT effectively protects against experimental ALI via activating the SIRT1/Nrf-2 pathway.