LPS诱发急性肺损伤中miR-16的表达及功能研究  

Expression and Function of miR-16 in Lipopolysaccharide-induced Acute Lung Injury

作　　者：才志刚[1] 张绍明[1] 张珩[1] 周宜勇[1] 吴海波[1] 徐小平[1] 

机构地区：[1]中国人民解放军第四五五医院心胸外科,上海200052

出　　处：《南昌大学学报（医学版）》2011年第2期1-5,共5页Journal of Nanchang University：Medical Sciences

基　　金：南京军区医学科研立项课题(09MA028)

摘　　要：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-α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-α的表达水平;在培养的肺上皮细胞A549中采用miR-16 mi mic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-α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-ɑ 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（P0.05）.Over-expression of miR-16（P0.01）in A549 cells significantly inhibited the expression of IL-6 and TNF-ɑ（P0.05）.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 miR-16 play an important role in inflammation following acute lung injury.

关 键 词：脂多糖 急性肺损伤 MICRORNAS miR-16 TNF-Α 炎症 动物 实验 小鼠 

分 类 号：R-332[医药卫生]