摘要
Abstract
Objective:To explore the effect of MYC-induced long non-coding RNA(MINCR)on neutrophil survival,migration,apoptosis,and cytokine production in pulpitis via the p38 mitogen-activated protein kinase(MAPK)signaling path-way.Methods:Human dental pulp fibroblasts were treated with 2 μg/mL lipopolysaccharide(LPS)and co-cultured with neu-trophils isolated from human peripheral blood.The neutrophils were divided into negative control short hairpin RNA group(sh-NC group),MINCR short hairpin RNA group(sh-MINCR group),negative control overexpression group(NC-OE group),the MINCR overexpression group(MINCR-OE group),and the MINCR overexpression+p38 inhibitor group(MINCR-OE+p38 inhibitor group).qRT-PCR was used to detect MINCR expression in cells from each group.Western blot was per-formed to detect phosphorylated(p)-p38 MAPK protein expression.CCK-8 method and Transwell chamber were used to de-tect cell viability and migration in cells from each group.Annexin V-PE/7-AAD double staining and cysteine-aspartic acid protease 3(Caspase-3)activity assay kit were performed to detect cell apoptosis.ELISA method was used to measure the lev-els of IL-1β,TNF-α,and IL-6.Results:After co-culture of LPS-treated human dental pulp fibroblasts with neutrophils,the expression of MINCR and p-p38 MAPK protein was significantly increased in neutrophils(P<0.05).Silencing MINCR ex-pression significantly reduced neutrophil viability,migration,and inflammatory factors,increased cell apoptosis,and inhibited p-p38 MAPK protein expression(P<0.05).Overexpression of MINCR significantly enhanced neutrophil viability,migration,and inflammatory factors,reduced cell apoptosis,and promoted p-p38 MAPK protein expression(P<0.05).Inhibition of p-p38 MAPK protein expression could reverse the effect of MINCR overexpression on neutrophil viability,migration,apoptosis,and inflammatory factors(P<0.05).Conclusion:MINCR influences neutrophil survival,migration,apoptosis,and the produc-tion of inflammatory factors in pulpitis by promoting the p38 MAPK signaling pathway.关键词
MYC诱导的长链非编码RNA/牙髓炎/p38丝裂原活化蛋白激酶/中性粒细胞/共培养体系Key words
MYC-induced long non-coding RNA/Pulpitis/p38 mitogen-activated protein kinase/Neutrophils/Co-culture system分类
医药卫生
