Remifentanil attenuates lipopolysaccharide-induced acute lung injury by downregulating the NF-κB signaling pathway.

Abstract

Remifentanil significantly represses cell immune responses and influences neutrophil migration through endothelial cell monolayers. The present study determines the beneficial effects of remifentanil and the mechanisms by which it attenuates lipopolysaccharide (LPS)-induced acute lung injury (ALI). Rats were intratracheally instilled with 2 mg/kg LPS to induce ALI. Results showed that remifentanil could resolve lung injury, as evidenced by remarkable decreases in lung edema (wet-to-dry weight ratio), neutrophil infiltration (myeloperoxidase activity), and pulmonary permeability [total number of cells and protein concentrations in bronchoalveolar lavage fluid (BALF)]. Remifentanil also attenuated the concentrations of proinflammatory cytokines tumor necrosis factor alpha, interleukin-1β, and interleukin-6 in BALF, as well as effectively repressed the activation of nuclear factor-kappaB (NF-κB), which has been associated with the inhibition of IκBα degradation.These results suggest that remifentanil may be a suitable treatment for LPS-induced ALI. Remifentanil exerts beneficial effects on the inhibition of proinflammatory cytokine production by downregulating the NF-κB pathway.