The expression of miR-876-3p based on a rat model of bronchopulmonary dysplasia induced by hyperoxia / 中国小儿急救医学

Objective:To establish a neonatal rat bronchopulmonary dysplasia(BPD) model induced by hyperoxia, to detect the expression of miR-876-3p in the lung tissue, and to analyze the role of miR-876-3p in the occurrence and development of BPD, so as to provide a theoretical basis for the pathogenesis, prevention and treatment of BPD.Methods:Eighty newborn SD rats were randomly divided into hyperoxia group(FiO 2 60%) and air group(FiO 2 21%). Lung tissue samples were taken on the 1st, 7th, 14th and 21st day after birth, the pathological changes of lung tissue were observed.Quantitative real-time PCR technique was used to detect the expression level of miR-876-3p. Results:Within 21 days after birth, with the prolongation of hyperoxia exposure time, the general growth of rats in hyperoxia group were lower than those in air group[14 d: (35.46±1.62) g vs.(37.08±1.25) g; 21 d: (51.92±1.83) g vs.(58.87±2.43) g]( P<0.05). On the 14th and 21st day after birth, the radial alveolar counts in lung tissue of rats in hyperoxia group were significantly reduced compared with those in air group( P<0.05). On the 7th, 14th and 21st day after birth, the alveolar septal thickness of rats in air group were lower than those in hyperoxia group( P<0.05). The expression level of miR-876-3p in hyperoxia group decreased gradually and was significantly lower on the 7th, 14th and 21st day compared with air group at the same time points[7 d: (14.97±1.13) vs.(16.64±0.89); 14 d: (11.92±0.71) vs.(16.85±0.79); 21 d: (11.39±0.79) vs.(17.52±1.17)], and the differences were all statistically significant( P all<0.01). Conclusion:In this study, a new BPD model of neonatal rats can be induced by hyperoxia and the expression level of miR-876-3p in this model is decreased.The differential expression level of miR-876-3p may play a role in the occurrence and development of BPD.

LINC00519 regulates the proliferation, apoptosis, migration and invasion of gastric cancer cells through the miR-876-3p/HMGA1 axis / 中国肿瘤生物治疗杂志

@#[摘 要] 目的：探讨长基因间非编码RNA 00519（long intergene non-coding RNA 00519，LINC00519）调控miR-876-3p/高迁移率家族蛋白A1（high mobility group protein A1，HMGA1）轴在胃癌HGC-27细胞的增殖、凋亡、迁移和侵袭中的作用。方法：采用qPCR检测胃癌细胞HGC-27和胃黏膜上皮细胞GES-1中LINC00519的表达水平。将HGC-27细胞按转染处理分为si-NC、si-LINC00519、si-LINC00519+anti-miR-NC和si-LINC00519+anti-miR-876-3p组，采用集落形成实验检测细胞克隆形成能力，流式细胞术检测细胞凋亡和周期分布，Transwell实验检测细胞迁移和侵袭。双荧光素酶报告实验和qPCR验证LINC00519与miR-876-3p、miR-876-3p与HMGA1之间的相互作用。结果：HGC-27细胞中LINC00519表达较GES-1细胞显著升高（P<0.05），转染siRNA后si-LINC00519组HGC-27细胞中LINC00519的表达水平较si-NC组显著降低（t=47.294，P<0.01）。与si-NC组比较，si-LINC00519组HGC-27细胞克隆数、迁移侵袭数、S期细胞比例均显著降低（均P<0.01），凋亡率、G0/G1期细胞比例均显著升高（均P<0.01）。与si-LINC00519+anti-miR-NC组比较，si-LINC00519+anti-miR-876-3p组HGC-27细胞克隆数、迁移侵袭数、S期细胞比例升高（均P<0.01），凋亡率、G0/G1期细胞比例显著降低（均P<0.01）。LINC00519能够靶向负调控miR-876-3p的表达，miR-876-3p靶向负调控HMGA1的表达。结论：敲降LINC00519能够通过调控miR-876-3p/HMGA1轴抑制胃癌HGC-27细胞的增殖、迁移和侵袭，诱导细胞凋亡。