LAUSR

The purpose of this study was to investigate the effect of desflurane (Des) pretreatment on sepsisevoked lung injury in rats and its mechanism. The rat model of sepsis-evoked lung injury was prepared using lipopolysaccharide (LPS), while rat lung mesenchymal cell (MSC) model was cultured in vitro, followed by Des pretreatment or inhibitor S31-201 culture. The degree of lung tissue injury was analyzed by Hematoxylin-eosin (HE) staining. The expression levels of interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α in the serum of rats were detected by enzyme-linked immunosorbent assay (ELISA). One-step terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was utilized to determine the apoptosis levels of lung tissues and MSCs cultured in vitro. The expressions of the signal transducer and activator of transcription 3 (STAT3) pathway in rat lung tissues and MSCs were detected by Western blotting. After modeling, LPS induced the lung injury in rats, the expression levels of IL-6, IL-1β and TNF-α were up-regulated (P<0.05), the apoptosis rate was increased (P<0.05), and phosphorylated-Janus kinase 2 (p-JAK2) and phosphorylated-STAT3 (p-STAT3) protein expressions were up-regulated (P<0.05). Des pretreatment can alleviate LPS-induced lung injury, down-regulate IL-6, IL-1β and TNF-α expression levels (P<0.05), reduce apoptosis (P<0.05), and downregulate p-JAK2 and p-STAT3 protein levels (P<0.05). LPS induced an increase in apoptosis rate of MSCs (P<0.05) and the up-regulation of p-STAT3 protein expression (P<0.05). Both Des pretreatment and S31-201 inhibitor culture could reduce the apoptosis rate (P<0.05) and down-regulate p-STAT3 protein level (P<0.05). Des pretreatment can reduce sepsis-evoked lung injury in rats, which may be related to the inhibition of protein expressions of STAT3 pathway.