Dexmedetomidine Attenuates LPS-Induced Acute Lung Injury in Rats by Activating the Nrf2/ARE Pathway

Background. To investigate the effect of dexmedetomidine (Dex) on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats and its mechanism. Methods. Eighteen SD rats were randomly divided into 3 groups (6 rats in each group): control group (intratracheal instillation of saline), ALI group (intratracheal instillation of 5 mg/kg LPS), and ALI-Dex group (tail vein injection of 50 mu g/kg/h Dex + intratracheal instillation of LPS). Subsequently, the water content of lung tissues was assessed using the wet-dry (W/D) ratio and the histopathological changes of lung tissues using H&E staining. Further activities of ROS, SOD, and GSH-Px in lung tissues of rats were measured by an automatic biochemistry analyzer. ELISA was performed to detect TNF-alpha, IL-1 beta, and IL-6 expression in alveolar lavage fluid (BALF) and Western blot to detect the expression of Nrf2/ARE pathway-related proteins. Results. After Dex treatment, a reduction in water content in lung tissue and an improvement of lung injury were found in the ALI rats. Compared with the ALI group, rats in the ALI-Dex group had decreased ROS activity and increased activities of SOD and GSH-Px in lung tissues. Dex-treated rats were also associated with a decrease in TNF-alpha, IL-1 beta, and IL-6 expression in alveolar lavage fluid (BALF). Additionally, increased expression levels of HO-1 and NQO1 in lung tissues and elevated expression of Nrf2 in the nucleus were shown in the ALI-Dex group compared with the ALI group. Conclusion. Dex alleviates LPS-induced ALI by activating the Nrf2/ARE signaling pathway.