β-defensin 2在肺缺血再灌注损伤中的表达及机制研究

The expression and mechanism of β-defensin 2 in lung ischemia reperfusion injury

目的探讨β-defensin 2在肺缺血再灌注损伤中的表达及机制。方法将16只SPF级雄性SD大鼠随机分成对照组(Control组)和肺缺血再灌注损伤组(LIRI组),LIRI组大鼠开胸,左肺缺血1 h,再灌注2 h,建立肺缺血再灌注损伤模型,Control组开胸2 h,收集左肺组织;细胞水平,肺泡Ⅱ型上皮细胞A549,分别缺氧0、4、24h,然后复氧2 h,建立细胞缺氧模型。采用HE染色,观察肺组织病理变化,计算肺组织的湿/干重比,ELISA方法检测肺组织中炎症因子的释放,qRT-PCR方法检测肺组织和上皮细胞中β-defensin 2的表达变化,Western blot方法检测肺组织和上皮细胞中p38MAPK信号通路的激活水平。结果肺缺血再灌注导致肺组织的急性炎症反应,β-defensin 2在肺组织和上皮细胞中表达上调,p38MAPK信号通路被激活。结论在肺缺血再灌注损伤中,β-defensin 2的表达上调,可能依赖于p38MAPK信号通路,参与肺组织的炎症应答反应。

Objective To investigate the expression and mechanism of β-defensin 2 in lung ischemia reperfusion injury.Methods At the animal level,sixteen SPF male Sprague-Dawley rats were randomly divided into two groups:the control group(Control group)and the lung ischemia reperfusion injury group(IRI group).The rats of the IRI group had thoracotomy and left lung ischemia for one hour and reperfusion for two hours,and a model of lung ischemia reperfusion injury was established.In the control group,the chest was opened for two hours to collect the left lung tissue;at the cellular level,the type Ⅱ alveolar epithelial cells A549 were hypoxic for 0 h,4 h,24 h,respectively,and then deoxygenated for two hours.A cell hypoxia model was established.HE staining was used for measuring the pathological changes of lung tissues.The wet/dry weight ratio of lung tissue was calculated and inflammatory cytokines in lung tissues were detected by ELISA.The expression of β-defensin 2 in lung tissue and epithelial cells was detected by qRT-PCR.The activation of p38 MAPK signaling pathway in lung and epithelial cells was detected by western blot.Results Lung ischemia reperfusion resulted in an acute inflammatory reaction in lung tissues,and β-defensin 2 was up-regulated in lung tissue and epithelial cell,and p38 MAPK signaling pathway was activated.Conclusion The up-regulation of β-defensin 2 in lung tissue after lung ischemia reperfusion may depend on the p38 MAPK signaling pathway involving in inflammatory reaction.