Sevoflurane reduces inflammatory factor expression, increases viability and inhibits apoptosis of lung cells in acute lung injury by microRNA-34a-3p upregulation and STAT1 downregulation.

OBJECTIVE

Evidence has shown that sevoflurane plays a protective role in acute lung injury (ALI) due to its anti-inflammatory and apoptotic-regulating activity. Nevertheless, the mechanism of sevoflurane is still not completely understood. This study intends to discuss the mechanism of sevoflurane on ALI and the possible mechanisms involved.

METHODS

ALI model of rats was established through intravenous injection of endotoxin lipopolysaccharide. microRNA-34a-3p (miR-34a-3p) and signal transducers and activators of transcription 1 (STAT1) expression in lung tissues of ALI rats were detected. The optimal inhaled concentration of sevoflurane was screened, and then the modeled rats were injected with miR-34a-3p inhibitors, overexpressed STAT1 and inhaled 1.0 Minimum Alveolar Concentration (MAC) sevoflurane to determine mean arterial pressure (MAP) of rats, wet weight/dry weight ratio and myeloperoxidase (MPO) activity, oxidative stress- and inflammation-related factors in lung tissues of rats, along with lung cell viability and apoptosis.

RESULTS

MiR-34a-3p was downregulated while STAT1 was upregulated in ALI rats. Sevoflurane of 1.0 MAC was selected as the optimal inhalation concentration. Sevoflurane (1.0 MAC) increased MAP at T3 and reduced MPO activity, alleviated pathological damage, suppressed apoptosis, oxidative stress and inflammation, and induced cell viability in lung tissues of ALI rats. Down-regulated miR-34a-3p or up-regulated STAT reversed the functions of sevoflurane (1.0 MAC) on ALI rats.

CONCLUSION

Collectively, we demonstrate that sevoflurane reduces inflammatory factor expression, increases lung cell viability and inhibits lung cell apoptosis in ALI through upregulation of miR-34a-3p and downregulation of STAT1, which provides new clues for ALI treatment.