Isoflurane suppresses lung ischemia-reperfusion injury by inactivating NF-κB and inhibiting cell apoptosis.

Abstract

Patients with lung ischemia-reperfusion injury (LIRI), involving cytokines, including interleukin (IL)-6 and IL-8, display poor clinical outcomes. Isoflurane displays protective effects against ischemia-reperfusion injury in numerous organs. In the present study, the effects of isoflurane on LIRI were investigated in vitro using a hypoxia-reoxygenation (HR) cell model. The mRNA expression levels of specific genes were analyzed by reverse transcription-quantitative PCR and protein expression levels were measured by ELISA and western blotting. Cell apoptosis and proliferation were assessed by flow cytometry and the Cell Counting Kit-8 assay, respectively. Isoflurane pretreatment decreased HR-induced IL-6 and IL-8 expression levels in A549 cells. Isoflurane pretreatment also inhibited HR-induced cell apoptosis and Bax expression, and reversed HR-induced downregulation of Bcl-2 expression. Moreover, isoflurane pretreatment decreased HR-induced NF-κB phosphorylated-p65 protein expression and NF-κB activation. Furthermore, HR-induced increases in malondialdehyde concentration and decreases in superoxide dismutase activity were reversed by isoflurane pretreatment. In conclusion, the results indicated that isoflurane suppressed LIRI by inhibiting the activation of NF-κB and the induction of cell apoptosis.