Abstract: Objective To investigate the effect and mechanism of ropivacaine (Rop) on lipopolysaccharide (LPS) -induced acute lung injury (ALI) in mice. Methods Mice with lung injury induced by endotracheal infusion of LPS were randomly divided into 6 groups: the control group, the LPS group, the Rop 0. 25 μmol / L group, the Rop 0. 5 μmol / L group, the Rop 1 μmol / L group and the dexmedetomidine ( Dex) 100 μg / kg group. Hematoxylin-eosin ( H&E) staining was used to evaluate histopathological changes of the lung tissues. The activities of myeloperoxidase (MPO) and malondialdehyde (MDA) in lung tissues of mice were determined by the colorimetric method. The levels of superoxide dismutase ( SOD) and glutathione peroxidase ( GSH-Px) in lung tissues, and the expression levels of interleukin ( IL) -6, IL-1β and tumor necrosis factor (TNF) -α in serum were assayed by ELISA. The expression levels of HMGB1 / NF-κB path- way related proteins were detected by Western blotting. Results The treatment of LPS induced the occurrence of hemorrhage and pulmonary edema in mice, and the thickening of alveolar membrane in lung tissues. The lung injury score and the water content in the lung tissues were increased in the LPS group when compared with the control group. The activities of MPO and MDA, the levels of IL-6, IL-1β and TNF-α in serum were increased in the LPS group, while the levels of SOD and GSH-Px were decreased. The expression level of HMGB1 protein was increased and the phosphorylation of NF-κB P65 were upregulated in the LPS group (P<0. 05). Compared with LPS group, the degree of lung injury in mice was significantly decreased, the activities of MPO and MDA, the levels of IL-6, IL-1β and TNF-α in serum were decreased, while the levels of SOD and GSH-Px were increased after Rop treatment. The expression level of HMGB1 protein was decreased and the phosphorylation of NF-κB P65 was downregulated in the Rop 0. 5 and 1 μmol / L groups (P<0. 05). Conclusion Rop effectively attenuates the LPS-induced lung injury by inhibiting HMGB1 / NF-κB pathway.

Key words: ropivacaine, lung injury, lipopolysaccharide, NF-κB