miR-142-5p对LPS诱导的小鼠乳腺上皮细胞炎性因子释放和增殖、凋亡的影响

Effects of MiR-142-5p on Lipopolysaccharide Induced Inflammatory Factors Release and Proliferation and Apoptosis of Murine Mammary Epithelial Cells

本试验旨在探讨miR-142-5p对脂多糖(LPS)诱导的小鼠乳腺上皮细胞炎性因子释放以及增殖和凋亡的影响。采用小鼠乳腺上皮细胞系经LPS诱发炎症反应,分别经miR-142-5p模拟物或抑制剂处理,检测细胞TNF-α、IL-1β、IL-6和IL-8的释放水平,AKT/p65信号通路关键蛋白磷酸化水平以及细胞增殖和凋亡水平。结果显示:与对照组比较,LPS组TNF-α、IL-6、IL-1β、IL-8分泌水平显著上调(P<0.05),p-AKT和p-P65蛋白相对表达水平显著上调(P<0.05),G0/G1期细胞比率上调,S期细胞比率降低,细胞增殖活力下降,细胞凋亡率显著增加(P<0.05);与LPS组相比,LPS+抑制剂组上述检测数值变化减弱(P<0.05),而LPS+模拟物组上述检测数值变化则进一步增强(P<0.05),LPS+抑制剂阴性对照组和LPS+模拟物阴性对照组上述检测数值均无显著差异(P>0.05)。结果表明,miR-142-5p可能通过激活AKT/p65信号通路,促进炎性因子的分泌和释放,并抑制细胞增殖,促进细胞凋亡。

This study aimed to investigate the effects of miR-142-5p on lipopolysaccharide(LPS) induced inflammatory factor release, proliferation and apoptosis of murine mammary epithelial cells. Specifically, LPS was used to induce inflammation in murine mammary epithelial cell line followed by treatment with miR-142-5p mimics and inhibitor, respectively, to detect the levels of TNF-α, IL-1β, IL-6 and IL-8, the phosphorylation levels of key proteins of AKT/p65 signaling pathway, and the levels of cell proliferation and apoptosis. The results showed that compared with those in the control group, the levels of TNF-α, IL-6, IL-1β and IL-8 as well as p-AKT and p-P65 in LPS group were significantly up-regulated(P<0.05), the ratio of G0/G1phase cells was up-regulated, the ratio of S phase cells was decreased, the proliferation activity of cells was decreased, and the apoptosis rate was significantly increased(P<0.05). Compared with those in LPS group, those in the LPS+inhibitors group were significantly inhibited(P<0.05);those in LPS+mimics group were further enhanced(P<0.05), and those in LPS + inhibitors NC group and LPS+mimics NC group were not significantly changed(P>0.05). Thus, miR-142-5p appears to promote the secretion and release of inflammatory factors, inhibit cell proliferation, and enhance cell apoptosis by activating AKT/p65 signal pathway.