脂多糖诱导的小鼠急性呼吸窘迫综合征中microRNA-27a和PPARγ表达变化

发布时间：2018-10-31 12:03

【摘要】：目的研究脂多糖(lipopolysaccharides,LPS)诱导小鼠急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)模型中外周血和肺内microRNA-27a和过氧化物酶体增殖物激活受体γ(peroxisome proliferators-activated receptor-γ,PPARγ)表达变化规律,探讨microRNA-27a和PPARγ在ARDS发病机制中的作用。方法将50只8~10周雄性C57BL/6小鼠分为模型组不同给药时间(3、6、12、24 h各10只)和对照组(n=10)。通过尾静脉注射LPS建立ARDS模型,通过组织学病理评价、炎症反应细胞分泌物表达水平等炎症反应指标评价ARDS模型建立的有效性。Western blot和免疫组织化学(IHC)观察模型不同时间点肺内PPARγ表达及变化趋势;实时荧光定量PCR(qRT-PCR)进一步研究基因表达改变情况。结果与对照组相比,模型组不同时间点肺组织病理改变明显;外周血和肺内不同时间点microRNA-27a表达明显增加,外周血各时间点较变化对照组增加2~4倍,差异有统计学意义[3 h(3.53±0.89),6 h(1.97±0.40),12 h(1.87±0.35),24 h(1.98±0.53),P0.05]。与对照组相比,肺内microRNA-27a 6 h(3.08±0.97)、24 h(3.49±0.94)表达增加差异有统计学意义;3 h(1.90±0.87)、12 h(1.88±0.62)差异无意义。PPARγ在蛋白水平表达明显减少;基因水平上外周血PPARγ6、12 h表达降低差异有统计学意义[P0.05,6 h(0.31±0.19),12 h(0.37±0.43)],3(0.70±0.33)、24 h(0.80±0.44)差异无统计学意义;肺内6、12、24 h表达降低差异有统计学意义[P0.05,6 h(0.60±0.23),12 h(0.71±0.12),24 h(0.42±0.20)],3 h(0.67±0.36)差异无统计学意义。结论 LPS诱导小鼠ARDS模型中,microRNA-27a和PPARγ表达发生明显变化,二者可能参与ARDS发病过程。
[Abstract]:Objective to study microRNA-27a and peroxisome proliferator-activated receptor 纬 (peroxisome proliferators-activated receptor- 纬) in peripheral blood and lung of lipopolysaccharide (lipopolysaccharides,LPS) induced acute respiratory distress syndrome (acute respiratory distress syndrome,ARDS) model in mice. To explore the role of microRNA-27a and PPAR 纬 in the pathogenesis of ARDS. Methods 50 male C57BL/6 mice were divided into two groups: model group (n = 10) and control group (n = 10). ARDS model was established by tail vein injection of LPS, and histologically and pathologically evaluated. Inflammatory response indexes such as the level of inflammatory response cell secretion were used to evaluate the effectiveness of ARDS model and immunohistochemical (IHC) to observe the expression and change trend of PPAR 纬 in lung at different time points. Real-time quantitative PCR (qRT-PCR) was used to further study the gene expression changes. Results compared with the control group, the pathological changes of lung tissue in the model group were obvious at different time points. The expression of microRNA-27a in peripheral blood and lung was significantly increased at different time points, and the expression of microRNA-27a in peripheral blood was significantly increased by 2 times than that in control group at different time points [3 h (3.53 卤0.89), 6 h (1.97 卤0.40)]. 12 h (1.87 卤0.35), 24 h (1.98 卤0.53), P0.05]. Compared with the control group, the expression of microRNA-27a in lung increased significantly at 6 h (3.08 卤0.97) and 24 h (3.49 卤0.94). There was no significant difference between 3 h (1.90 卤0.87) and 12 h (1.88 卤0.62). The expression of PPAR 纬 was significantly decreased at the protein level. At the gene level, there was no significant difference in the expression of PPAR 纬 at 12 h in peripheral blood [(0.31 卤0.19), (0.37 卤0.43)], (3) (0.70 卤0.33), (0.80 卤0.44) h (P 0.05), (0.31 卤0.19), (0.37 卤0.43), (0.80 卤0.44), respectively. There was no significant difference in 24 h expression of 6H ~ (12) P ~ (0.05) h (0.60 卤0.23), 12 h (0.71 卤0.12), 24 h (0.42 卤0.20), 3 h (0.67 卤0.36). Conclusion the expression of microRNA-27a and PPAR 纬 in ARDS model induced by LPS is obviously changed, which may be involved in the pathogenesis of ARDS.
【作者单位】：第三军医大学西南医院呼吸内科;第三军医大学大坪医院野战外科研究所呼吸内科;第三军医大学基础医学部生物化学与分子生物学教研室;
【基金】：国家自然科学基金面上项目(81670070)~~
【分类号】：R563.8

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