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Fluorofenidone Attenuates SiO2 Induced Pulmonary Fibrosis in Mice Via Inhibiting IL-1β Signaling Pathway

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A1068 - Fluorofenidone Attenuates SiO2 Induced Pulmonary Fibrosis in Mice Via Inhibiting IL-1β Signaling Pathway
Author Block: J. Meng1, T. Luo2; 1Dept of Respiratory and Critical Care Medicine, Dept of Respiratory Medicine, Key cite of, Xiangya Hospital, Central South University, Changsha, China, 2Department of Respiratory and Critical Care Medicine?Department of Respiratory Medicine??Key cite of, Xiangya Hospital, Central South University, Changsha, China.
Objective: Silicosis is a chronic fibrotic lung disease caused by inhalation of free crystalline silicon dioxide or silica. As yet, there no effective treatment for silicosis, and the mechanisms of silica crystal induced lung inflammation and fibrosis are not well understood. Aim: To detect whether fluorofenidone showed the antifibrotic effect in silicosis of mice by inhibiting IL-1β pathway.Methods: Twenty-four C57BL/6J mice were randomly divided into three groups : the control group (Control), the SiO2 group (SiO2), the SiO2/ fluorofenidone group . The model of silicosis was established through intratracheal administration with SiO2 suspension (1 mg/kg) while Control group by instillation the same dose of normal saline. 24 hrs before establishment of the model, the fluorofenidone group was fed with fluorofenidone (500 mg/kg, once per day) while Control group fed with the same dose of normal saline. Stochastically, eight mice in each group were killed after 28 days. The pathology changes were evaluated by hemotoxylin and eosin stain and Masson's trichrome stain, a-smooth muscle actin (a-SMA), fibronectin, caspase-1, IL-1β were measured by Western blotting analyses.Results: Compared with SiO2 group,(1) fluorofenidone group could relieve the fibrotic changes and inflammation in lung of mice; (2) fluorofenidone remarkly reduced the express of a-smooth muscle actin (a-SMA), fibronectin, caspase-1, IL-1β.Conclusions: AKF-PD attenuates SiO2-induced pulmonary inflammation and fibrosis through suppressing the IL-1β signaling pathway.
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