摘要
目的:通过观察地塞米松对大鼠肺缺血再灌注后内皮型一氧化氮合酶(eNOS)的影响探讨其对缺血再灌注肺的保护机制。方法:40只健康SD大鼠,雌雄不拘,随机分为5组:假手术组(S)、单纯缺血组(I)、缺血再灌注组(IR)、小剂量地塞米松干预组(D1)及大剂量地塞米松干预组(D2),每组8只。根据Eppinger模型制作SD大鼠单侧肺IRI动物模型,Western-blot法检测eNOS蛋白质浓度,HE染色观察组织病理学改变。结果:与其它组比较,IR组肺组织中eNOS表达明显下降(P<0.01),地塞米松干预后,eNOS表达明显增高,以D2组明显。病理切片示IR组肺组织结构损害分级显著重于其它组,地塞米松干预后肺组织结构损害分级下降,以D2组明显。结论:eNOS在正常肺组织中表达较多,IR可使eNOS表达明显下降,地塞米松可使eNOS表达增高,尤以大剂量时明显,地塞米松通过上调eNOS表达减轻缺血再灌注肺组织损伤。
Objective:To explore the protective effect of Dexamethasone by observing the change of eNOS protein in the case of pulmonary ischemia-reperfusion before and after the intervention of Dexamethasone in rats.Methods:40 health Sprague-Dawley rats were chosen without considering of their sexes,they were divided randomly into five groups:Sham group(S),ischemia-only group(I),ischemia-reperfusion group(IR),small-dose dexamethasone intervened group(D1),large-dose dexamethasone intervened group(D2),with eight in each group.Rat model of warm ischemia and reperfusion in situ in single lung was prepared on the basis of Eppinger Model.The protein of eNOS in lung tissue was detected by Western blot,and pulmonary pathological changes were observed by HE staining.Result:Compared with other groups,the expression of eNOS protein in Group IR was much lower(P0.01),which increased after the intervention of Dexamethasone,especially in large dose.The pathological section showed that the pulmonary structural lesion was more serious in Group IR,and the structural lesion was lessened after the intervention of Dexamethasone.Conclusion:The expression of eNOS in normal lung tissue is high,but if the lung is ischemia-reperfusioned,the eNOS decreases obviously while the lung injury is obvious.After the intervention of Dexamethasone,especially in large dose,the eNOS protein increases and Kaminski A,Pohl CB,Sponholz C,the lung injury lessens.
出处
《南通大学学报(医学版)》
2010年第1期61-62,65,F0003,共4页
Journal of Nantong University(Medical sciences)
基金
南通市社会发展基金资助(S2008017)
关键词
缺血再灌注
肺
地塞米松
内皮型一氧化氮合酶
大鼠
Ischemia-reperfusion
Lung
Dexamethasone
Epithelial nitrix oxide synthase
Rat