Background
Acute lung injury (ALI) is a common clinical complication with a high mortality rate. Resveratrol (Res) has been shown to protect against ALI, but the role of long noncoding RNAs (lncRNAs) in this process is still unclear.
Conclusions
Res can inhibit the increase of lncRNAs XLOC_014869 caused by LPS stimulation and inhibit lung cell apoptosis. These effects may be due to lncRNA XLOC_014869 mediation of the pro-apoptotic factors (Fos, c-Jun, and Fas-L).
Methods
Male rats (n=20) aged 7-8 weeks were randomly divided into four groups: control, lipopolysaccharide (LPS), LPS + Res, and LPS + dexamethasone (Dexa). Intragastric administration of Res (0.5 mg/kg) or Dexa (1.5 mg/kg) was performed 1 h before intraperitoneal injection of LPS (5 mg/kg). Lung tissue, serum, and bronchoalveolar lavage fluid were sampled 6 h after LPS treatment for inflammatory factor detection, pathological detection, lncRNA sequencing and bioinformatical analysis, and TdT-mediated dUTP Nick-End Labeling. Quantitative real time polymerase chain reaction and western blotting were used to verify the sequencing
Results
Res pretreatment inhibited lung injury and the increase of inflammatory cytokines induced by LPS. The differentially expressed lncRNAs and mRNAs (P<0.05 and |fold change| >2) were mainly involved in the signaling pathway of immunity, infection, signaling molecules and interactions. Among the lncRNAs and mRNAs, 26 mRNAs and 23 lncRNAs had high levels in lungs treated with LPS but decreased with Res, and 17 mRNAs and 27 lncRNAs were at lower levels in lungs treated with LPS but increased with Res. lncRNA and adjacent mRNA analysis showed that lncRNAs XLOC_014869 and the adjacent gene Fos, and the possible downstream genes Jun and Faslg were increased by LPS, but these changes were attenuated by Res. Pretreatment with Res reduced LPS-induced lung tissue apoptosis. Similarly, Res treatment and knockdown of lncRNA XLOC_014869 reduced LPS-induced apoptosis and the levels of Fos, c-Jun, and Fas-L. Conclusions: Res can inhibit the increase of lncRNAs XLOC_014869 caused by LPS stimulation and inhibit lung cell apoptosis. These effects may be due to lncRNA XLOC_014869 mediation of the pro-apoptotic factors (Fos, c-Jun, and Fas-L).