OBJECTIVE: To study the effect and mechanism of sodium ferulate (SF) in preventing and treating ozone (O3) induced lung oxidative injury in mice. METHODS: Lung oxidative injury model mice were established by making them inhale O3. The activity of anti-oxidase and membranous microviscosity in epithelial cells in the lung of mice were determined, and the ultrastructural change of lung tissues was observed with electromicroscopy. RESULTS: Activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were reduced, while membranous lipo-microviscosity significantly increased in the pulmonary epithelial cells of model mice, revealing ultrastructural change. These abnormal changes were reversed by SF treatment, which was manifested as the significantly raised activities of SOD and GSH-Px after treatment with high and moderate doses of SF, showing a significant difference compared with those in the model group (P<0.01). Membranous lipo-microviscosity basically approached that in the control group (P>0.05); electron microscopic examination showed a basically normal morphological structure of pulmonary epithelial cells, with the change in lung injury significantly milder than that in the model group. CONCLUSION: O3 could induce oxidative injury of lungs in mice, and SF could enhance the anti-oxidation capacity of mice and scavenge the oxygen free radicals so as to alleviate the injury.
OBJECTIVE: To study the effect and mechanism of sodium ferulate (SF) in preventing and treating ozone (O3) induced lung oxidative injury in mice. METHODS:Lung oxidative injury model mice were established by making them inhale O3. The activity of anti-oxidase and membranous microviscosity in epithelial cells in the lung of mice were determined, and the ultrastructural change of lung tissues was observed with electromicroscopy. RESULTS: Activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were reduced, while membranous lipo-microviscosity significantly increased in the pulmonary epithelial cells of model mice, revealing ultrastructural change. These abnormal changes were reversed by SF treatment, which was manifested as the significantly raised activities of SOD and GSH-Px after treatment with high and moderate doses of SF, showing a significant difference compared with those in the model group (P<0.01). Membranous lipo-microviscosity basically approached that in the control group (P>0.05); electron microscopic examination showed a basically normal morphological structure of pulmonary epithelial cells, with the change in lung injury significantly milder than that in the model group. CONCLUSION: O3 could induce oxidative injury of lungs in mice, and SF could enhance the anti-oxidation capacity of mice and scavenge the oxygen free radicals so as to alleviate the injury.