Effect of miR-126 on rats with acute lung injury by regulating MAPK/NF-κB signaling pathway
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.
acute lung injurymicroRNA-126mitogen activated protein kinasenuclear factor kappa Bintervention effect
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维普
