Aucubin Prevents Lipopolysaccharide-induced Acute Lung Injury in Mice via Inhibiting Inflammatory Response, Oxidative Stress and Apoptosis

The aim of this study was to investigate the effects of aucubin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Forty-eight mice were randomly divided into control, model, and aucubin groups. The aucubin group was given 10 mg/kg aucubin. After 1 h from treatment, the LPS-induced ALI model was constructed in model and aucubin groups. After 12 h from ALI modeling, the lung index and lung wet-dry mass ratio (W/D), bronchoalveolar lavage fluid (BALF) indexes, lung tissue oxidative stress indexes and lung tissue B-cell lymphoma-2 (Bcl-2) and B-cell lymphoma-2 associated X (Bax) protein expressions were determined. Results showed that, compared with model group, in aucubin group the lung index and lung W/D were decreased (P < 0.05), the BALF total protein concentration and percentage of PMN were decreased (P < 0.05), the BALF tumor necrosis factor a and interleukin 1 beta levels were decreased (P < 0.05), the lung tissue superoxide dismutase and glutathione levels were increased (P < 0.05), the lung tissue reactive oxygen species and malondialdehyde levels were decreased (P < 0.05), the lung tissue Bcl-2 protein expression level was increased (P < 0.05), and the lung tissue Bax protein expression level was decreased (P < 0.05). In conclusion, the aucubin pretreatment can alleviate the ALI in mice. The mechanisms may be related to its inhibiting inflammatory response, oxidative stress and apoptosis in lung tissues.