RÉSUMÉ
Objective To evaluate the protective effect of sevoflurane preconditioning on lung ischemia-reperfusion injury (IRI) and its influence on the Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor (NF)-κB signaling pathway. Methods Forty healthy adult SD rats were randomly divided into the control group (Sham group), lung IRI model group (LIRI group), sevoflurane group (Sev group) and TLR4 inhibitor TAK-242 combined with sevoflurane group (TAK+Sev group), 10 rats in each group. The pathological changes of lung tissues were observed by hematoxylin-eosin (HE) staining and the pathological injury score was graded. The cell apoptosis of lung tissues was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick- end labeling (TUNEL) and the apoptosis rate was calculated. The wet-to-dry (W/D) ratio of lung tissues was measured to determine the water content of lung tissues. The levels of oxidative stress-related parameters in the lung tissues and inflammatory factors in both the lung tissues and serum were detected. The expression levels of TLR4/MyD88/NF-κB signaling pathway-associated proteins in the lung tissues were determined by Western blot. Results Compared with the Sham group, the pathological injury score, W/D ratio, cell apoptosis rate, malondialdehyde (MDA) level, inflammatory factor level and the relative expression levels of TLR4, MyD88 and NF-κB p65 proteins in the lung tissues were significantly increased, whereas the superoxide dismutase (SOD) level and the relative expression level of NF-κB inhibitory protein α(IκBα) were significantly decreased in the LIRI and Sev groups (all P < 0.05). Compared with the LIRI group, the pathological injury score, W/D ratio, cell apoptosis rate, MDA level, inflammatory factor level and the relative expression levels of TLR4, MyD88 and NF-κB p65 proteins were significantly decreased, whereas the SOD level and the relative expression level of IκBα were significantly increased in the Sev and TAK+Sev groups (all P < 0.05). Compared with the Sev group, the pathological injury score, W/D ratio, cell apoptosis rate, MDA level, inflammatory factor level and the relative expression levels of TLR4, MyD88, NF-κB p65 proteins were significantly decreased, while the relative expression level of IκBα was significantly increased in the TAK+Sev group (all P < 0.05). Conclusions Sevoflurane preconditioning may inhibit the activation of TLR4/MyD88/NF-κB signaling pathway and suppress inflammatory reaction and oxidative stress, thereby effectively mitigating the lung IRI.