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Abstract: Objective To investigate the influence of long non-coding RNA ( LncRNA) nuclear-enriched abundant transcript 1 ( NEAT1) on the biological activity of human gingival fibroblasts (HGFs) induced by lipopolysaccharide (LPS) by regulating miR-22-3p. Methods HGFs cells in logarithmic growth phase were grouped into 6 groups: control group, LPS group, si-NC group, si-Neat1 group, si-Neat1 + inhibitor NC group, and si-Neat1 + miR-22-3p inhibitor group. RT-qPCR was applied to detect the expression levels of Neat1 and miR-22-3p. Dual luciferase reporter assay was applied to verify the targeting relationship of Neat1 and miR-22-3p. Flow cytometry, CCK-8, and ELISA were used to detect apoptosis, cell viability, and levels of tumor necrosis factor-α (TNF-α) and interleukin-1β ( IL-1β), respectively. Western blotting assay was applied to detect the expression levels of caspase-3and NF-κB P65, and the phosphorylation level of NF-κBP65 (p-NF-κB P65). Results The cell viability and the expression level of miR-22-3p in the LPSgroup were significantly decreased, while the TNF-α, IL-1β, apoptosis rate, the levels of p-NF-κB P65 / NF-κB P65, Neat1, and Caspase-3 were significantly increased (P < 0. 05), when compared with those in the control group. The cell viability and the expression level of miR-22-3p in the si-Neat1 group were significantly increased, while the TNF-α, IL-1β, apoptosis rate, the levels ofp-NF-κB P65 / NF-κB P65, Neat1and Caspase-3 were significantly decreased ( P < 0. 05), when compared with those in the LPS group and the si-NC group. Down-regulation of miR-22-3p expression reversed the effect of Neat1 silencing on the biological activity of LPS-induced HGFs ( P <0. 05). Conclusion Silencing Neat1 can inhibit the apoptosis and inflammatory response of HGFsinduced by LPS, the mechanism may be related to the up-regulation of miR-22-3p expression.

Key words: LncRNA Neat1, miR-22-3p, lipopolysaccharide, human gingival fibroblasts;biological activity