摘要
目的 分析微小RNA-126(microRNA-126,miR-126)通过调控丝裂原活化蛋白激酶(MAPK)/核转录因子κB(NF-κB)信号通路对急性肺损伤大鼠的干预效果.方法 选取50只Wistar大鼠,10只作为对照组,不做任何处理,其余40只建立急性肺损伤模型,将建模成功30只大鼠分为模型组、miR-126沉默组、miR-126过表达组,每组10只.观察各组大鼠一般情况、病理组织学、miR-126表达量、氧化应激指标、血气分析指标、炎性因子、p38 MAPK、NF-κB p65 mRNA信号通路相关mRNA表达量、MAPK/NF-κB信号通路.结果 与对照组比较,模型组肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、p38 MAPK mRNA、NF-κB p65 mRNA、p38 MAPK、NF-κB p65 升高,miR-126、超氧化物歧化酶(SOD)活性、血氧分压(PaO2)降低(P＜0.05);与模型组比较,miR-126沉默组TNF-α、p38 MAPK mRNA、NF-κB p65 mRNA、p38 MAPK、NF-κB p65 升高,miR-126、SOD 活性、PaO2 降低,miR-126 过表达组 TNF-α、IL-1β、p38 MAPK mRNA、NF-κB p65 mRNA、p38 MAPK、NF-κB p65 降低,miR-126、SOD 活性、PaO2 升高(P＜0.05).结论 过表达 miR-126 可抑制MAPK/NF-κB信号通路的表达,降低炎性反应,改善大鼠氧化应激指标、血气分析指标及病理学变化.
Abstract
Objective To analyze the effect of microRNA-126(miR-126)on rats with acute lung injury(ALI)by regulating mitogen-activated protein kinase(MAPK)/nuclear factor kappa B(NF-κB)signaling pathway.Methods Fifty Wistar rats were selected and the remaining 40 rats were used to establish ALI model.Thirty rats with successful modeling were divided into model group(n=10),miR-126 silencing group(n=10)and miR-126 overexpression group(n=10),and the remaining 10 rats were selected as the control group without special treatment.The key observation was general condition of rats,pathological histology,miR-126 expression,oxidative stress indexes,blood gas analysis indexes,inflammatory factors,p38 MAPK,NF-κB p65 mRNA expression,and MAPK/NF-κB signaling pathway.Results The rats in the model group presented significantly increased levels of tumor necrosis factor-α(TNF-α),interleukin-1 β(IL-1β),p38 MAPK mRNA,NF-κB p65 mRNA,p38 MAPK and NF-κB P65,but significantly decreased miR-126,superoxide dismutase(SOD)activity,partial pressure of blood oxygen(PaO2)than those of control group(P＜0.05).The rats in the miR-126 silencing group had significantly increased levels of TNF-α,p38 MAPK mRNA,NF-κB p65 mRNA,p38 MAPK and NF-κB P65,but significantly decreased miR-126,SOD activity,PaO2 than those of model group(P＜0.05).The rats in the miR-126 overexpression group presented significantly decreased levels of TNF-α,IL-1β,p38 MAPK mRNA,NF-κB p65 mRNA,p38 MAPK and NF-κB P65,but significantly increased miR-126,SOD activity,PaO2 than those of model group(P＜0.05).Conclusion The miR-126 overexpression can reduce inflammatory response and improve oxidative stress indexes,blood gas analysis indexes and pathological changes in rats by inhibiting the expression of MAPK/NF-κB signaling pathway.
维普
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