LAUSR

OBJECTIVE Acute lung injury (ALI) is one of the most serious complications of sepsis and remains refractory. It is of great significance to discuss the pathogenesis of acute lung injury in sepsis and look for more effective drugs for treatment. The purpose of this study was to investigate the role of LincRNA-p21 on acute lung injury in sepsis. MATERIALS AND METHODS Lung histology was detected by HE staining to evaluate sepsis-induced ALI model in rats. The miRNA expression of LincRNA-p21 in septic model in vivo and in vitro was detected by RT-qPCR. Cell apoptosis, inflammatory responses and oxidative stress were detected to uncover the influence of LincRNA-p21 on LPS-induced septic model in vitro. RESULTS The expression of LincRNA-p21 was significantly increased in septic model in vivo and in vitro. Cell apoptosis, inflammatory responses and oxidative stress were alleviated by LincRNA-p21 interference in LPS-treated BEAS-2B cells. CONCLUSIONS All the results in the current study proved that LincRNA-p21 interference could alleviate the acute lung injury in septic model. It raised the conclusion that LincRNA-p21 may act as a novel regulator in the pathological process and a potential therapeutic target in sepsis-induced ALI.