摘要
目的探讨不规则趋化因子(FKN)在大鼠急性肺栓塞(APE)后的表达及其作用机制。方法采用自体血栓回输法复制Sprague-Dawley大鼠APE模型;将72只大鼠分为对照组、溶剂组、APE组,每组24只,观察1、4、8h3个时间点各组大鼠肺组织中磷酸化p38、FKN mRNA及蛋白表达情况。结果免疫组织化学检测显示,FKN、p38在APE组大鼠肺实质、肺动脉血管壁上均有明显表达;Western blot检测显示,APE组各时间点大鼠肺组织中磷酸化p38表达水平较对照组、溶剂组各时间点明显升高(P<0.05);RT-PCR检测结果显示,APE组各时间点大鼠肺组织中FKN mRNA表达水平较对照组、溶剂组各时间点升高(P<0.05)。结论APE后大鼠肺组织内FKN、p38的表达明显升高,可能p38丝裂原活化蛋白激酶(p38MAPK)信号通路在APE后FKN的表达中发挥调控作用。
Objective To observe the expression and mechanism of fractalkine(FKN)in acute pulmonary embolism(APE)rats.Methods The APE model of Sprague-Dawley rats was replicated by autologous thrombus transfer.A total of 72 rats were divided into the control group,the solvent group and the APE group,with 24 rats in each group.Observed the expression of phosphorylated p38 and FKN mRNA and protein in lung tissues of rats in the time points 1,4,8 h.Results Immunohistochemistry showed that FKN and p38 were significantly expressed in the lung parenchyma and pulmonary artery wall in the APE group.Western blot showed that the expression level of phosphorylated p38 in the APE group was higher than that in the control group and the solvent group at any time point(P<0.05);RT-PCR showed that the expression of FKN mRNA in the APE group was higher than that in the control group and the solvent group(P<0.05).Conclusion The expression of FKN and p38 in lung tissue of rats significantly increased after APE.The p38 mitogen-activated protein kinase(p38MAPK)signaling pathway may play a regulatory role in the expression of FKN after APE.
作者
谢小娜
蔡学定
XIE Xiaona;CAI Xueding(Department of Respiratory,Wenzhou Hospital of Traditional Chinese Medicine Affiliated Zhejiang Chinese Medical University,Wenzhou,Zhejiang 325000,China;Department of Respiratory and Critical Care Medicine,the First Affiliated Hospital of Wenzhou Medical University,Wenzhou,Zhejiang 325000,China)
出处
《重庆医学》
CAS
2018年第32期4112-4114,4118,共4页
Chongqing medicine
基金
浙江省温州市科技局项目(Y20130238)
