Abstract: Objective To investigate the regulatory mechanism of long-chain noncoding RNA metastasis-associated lung adenocarcinoma 1 (lnc-MALAT1) in the inflammatory response of lipopolysaccharide (LPS)-induced alveolar macrophages (AMOs). Methods AMOs cells were treated with LPS for 12 hours to create an inflammation model, and liposome method was used to transfect pcDNA, pcDNA-MALAT1, miR-NC, miR-217 mimics, pcDNA-MALAT1 and miR-NC, pcDNA-MALAT1 and miR-217 mimics to AMOs. The level of IL-1β and TNF-α was detected by ELISA. RT-qPCR was used to detect the expression of MALAT1 and miR-217 in cells. The dual luciferase report experiment and RIP experiment were used to detect potential target-attacking relationship between MALAT1 and miR-217. Results Compared with the AMOs group, the expression of IL-1β and TNFα, MALAT1 in the cells of the LPS+AMOs group were significantly increased (P＜0.05) and the expression level of miR-217 was significantly reduced(P＜0.05). The dual luciferase report experiment and RIP experiment confirmed that MALAT1 targeted at miR-217. Over-expression of MALAT1 could obviously promote the secretion of IL-1β and TNF-α induced by LPS in AMOs, while over-expression of miR-217 inhibited the secretion of IL-1β and TNF-α induced by LPS in AMOs. Furthermore, over-expression of miR-217 reduced the secretion of IL-1β and TNF-α induced by MALAT1 in LPS-induced AMOs. Conclusions Lnc-MALAT1, a long non-coding RNA, can promote the inflammatory response of AMOs induced by LPS, and its mechanism is related to its targeting at miR-217.

Key words: lnc-MALAT1, alveolar macrophages, miR-217, lipopolysaccharide(LPS)