Objective To investigate the effects of long non-coding RNA(lncRNA)SNHG15 on lipopolysaccharide(LPS)-induced injury of human alveolar epithelial cells and the underlying molecular mechanism.Methods A549 cells were treated with LPS to construct a neonatal acute respiratory distress syndrome(NRDS)cell model.A549 cells were divided into Control group,LPS group,LPS+si-NC group,LPS+si-lncRNA SNHG15 group,LPS+miR-NC group,LPS+miR-942-5p group,LPS+si-lncRNA SNHG15+anti-miR-NC group and LPS+si-lncRNA SNHG15+anti-miR-942-5p group.Real-time fluorescence quantitative PCR(qRT-PCR)was used to detect the expression levels of lncRNA SNHG15 and miR-942-5p.Flow cytometry and Western blot were conducted to detect cell apoptosis.ELISA was used to detect the expression levels of interleukin-6(IL-6),in-terleukin-1β(IL-1β),and tumor necrosis factor-α(TNF-α).Dual-luciferase reporter assay was used to identify the targeting rela-tionship between lncRNA SNHG15 and miR-942-5p.Results Compared with the Control group,lncRNA SNHG15 expression,apoptosis rate,and levels of Bax,IL-6,IL-1β and TNF-α were increased in the LPS group,while miR-942-5p expression and Bcl-2 protein level were decreased(all P＜0.05).After knockdown of lncRNA SNHG15 or overexpression of miR-942-5p,cell apop-tosis rate and levels of Bax,IL-6,IL-1β and TNF-α were decreased,while Bcl-2 level was increased(all P＜0.05).lncRNA SNHG15 targeted miR-942-5p,and downregulation of miR-942-5p reversed the effect of lncRNA SNHG15 knockdown on LPS-induced A549 cell injury(all P＜0.05).Conclusion Silencing of lncRNA SNHG15 alleviates LPS-induced A549 cell injury by upregulation of miR-942-5p.
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