Effect of the propofol on the NLRP3 signaling pathway in mice with acute lung injury

ObjectiveTo analyze the protective effects of propofol on the acute lung injury induced by lipopolysaccharide(LPS)and expression levels of thioredoxin-interacting protein(TXNIP)and nucleotide-binding domain-like receptor protein 3(NLRP3), and explore the possible mechanisms of lung protection with propofol.

MethodsForty ICR mice were divided into the control group(treatment with intraperitoneal injection of pH 7.4 phosphate buffer), LPS group(treatment with intraperitoneal injection of 30 mg/kg LPS), propofol group(treatment with intravenous injection of 40 mg/kg propofol)and propofol +LPS group(treatment with intraperitoneal injection of 30 mg/kg LPS after 20 min of intravenous injection of 40 mg/kg propofol)(10 mice in each group).The pathological analysis of lung tissue was conducted under light microscope, and the MDA content, SOD activity and expression levels of TXNIP and NLRP3 in pulmonary epithelial cells were detected.

ResultsThe lung histopathological results showed that propofol could significantly reduced the acute lung injury induced by LPS in mice.Compared with the control group, the MDA content and SOD activity in the lung tissues of LPS group were significantly increased and decreased, respectively(P < 0.01), and the expression levels of TXNIP, NLRP3 mRNA and protein were significantly up-regulated in LPS group(P < 0.01).Compared with the LPS group, the MDA content and SOD activity were significantly decreased and increased in the propofol+LPS group, respectviely(P < 0.01), and the expression levels of TXNIP and NLRP3 mRNA and protein in lung tissues of propofol+LPS group were significantly down-regulated(P < 0.01).

ConclusionsThe intravenous preinjection of propofol can down-regulate the mRNA and protein expressions of TXNIP and NLRP3 in lung tissues, effectively alleviate the acute lung injury induced by LPS, and play a protective role in lung tissue.