目的 观察脂多糖(LPS)诱发的急性肺损伤中microRNA-16 (miR-16) 的表达变化及其对炎症因子TNF-ɑ等表达的调节.方法 通过生物信息学分析不同物种间miR-16基因序列的保守性.通过小鼠气道向其肺内注入LPS(10 mg·kg-1),构建小鼠急性肺损伤模型,采用实时荧光定量PCR分析miR-16、IL-6、TNF-ɑ的表达水平;在培养的肺上皮细胞A549中采用miR-16 mimic对miR-16进行过表达研究.结果 miR-16基因序列在斑马鱼、大鼠、小鼠和人中序列高度保守;miR-16在急性肺损伤病理过程中表达明显降低(P＜0.05);A549细胞中miR-16的表达水平显著升高(P＜0.01),相反,LPS诱导的炎症因子IL-6、TNF-ɑ的表达水平显著降低(P＜0.05).结论 miR-16在LPS诱发的急性肺损伤病理过程中的表达降低,miR-16过表达能够显著抑制LPS对炎症的诱发作用,表明miR-16在急性肺损伤的炎症发生过程中发挥着重要功能.%Objective To observe the expression of microRNA-16 (miR-16) in lipopolysaccharide(LPS)-induced acute lung injury and to explore the role of miR-16 in the regulation of inflammatory cytokine expression. Methods The sequences of miR-16 were analyzed by using bioinformatics. LPS (10 mg · kg-1 )was intratracheally administered to induce acute lung injury in mice.A549 cells were transfected with miRNA mimic to explore the effect of miR-16 on inflammatory reaction. The levels of miR-16,IL-6 and TNF-a expression were determined by real-time PCR.Results MiR-16 was evolutionarily conserved in zebrafish,rats,mice and humans. In LPS-induced lung injury model, miR-16 expression was profoundly down-regulated(P＜0.05). Over-expression of miR-16 (P＜0.01)in A549 cells significantly inhibited the expression of IL-6 and TNF-a(P＜0.05). Conclusion MiR-16 is aberrantly expressed in LPS-induced lung injury and over-expression of miR-16 inhibits inflammatory reaction induced by LPS in A549 cells,indicating that miR16 play an important role in inflammation following acute lung injury.
展开▼
