地塞米松对大鼠肺缺血再灌注损伤保护探究.docVIP

地塞米松对大鼠肺缺血再灌注损伤保护探究 　 作者：许文景 倪松石，黄冬云 【摘要】 目的:通过观察地塞米松对大鼠肺缺血再灌注后病理形态变化的影响，探讨其对肺缺血再灌注损伤的保护机制。方法:健康的SD大鼠40只，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大鼠单侧肺缺血再灌注动物模型，用Western 印迹法分析各实验组中一氧化氮合酶蛋白表达的变化，HE染色观察肺组织病理形态学改变 结果: 与其它组比较，缺血再灌注组肺组织中蛋白一氧化氮合酶表达明显增高（P＜0.01)，在地塞米松干预后，一氧化氮合酶蛋白下降，以D2组明显，病理切片显示IR 组肺结构损害分级显著重于其它组，在地塞米松干预后， 肺结构损害分级下降，以D2组明显。结论:正常肺脏一氧化氮合酶蛋白的表达微弱, 缺血再灌注可使一氧化氮合酶蛋白表达增加，肺组织损伤加重，地塞米松可使一氧化氮合酶蛋白表达下降，肺组织损伤减轻，这种效应以大剂量时明显。 【关键词】 缺血再灌注；肺； 地塞米松；一氧化氮合酶；大鼠 [Abstract] Objective: To explore the protective effect of Dexamethasone by observing the diversity of pathological appearance in the case of ischemia-reperfusion-induced pulmonary injury before and after the intervention of Dexamethasone in rats. Methods: 40 healthy Sprague-Dawley rats were chosen without considering of their sexes, and divided randomly into five groups: sham group（S）, ischemia-only group（I）, ischemia-reperfusion group （IR）, small-dose Dexamethasone interfered group （D1）, and large-dose dexamethasone interfered 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 inducible nitric oxide synthase (iNOS )in lung tissue was detected by Western-blot. Pulmonary pathological changes were observed by H-E staining. Result: Compared with other groups, the expression of iNOS protein in Group IR was much higher(P＜0.01),which decreased 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 after intervention, the structural lesion was lessened .Conclusion: The expression of iNOS protein in normal lung is little ,but if the lung is ischemia-reperfusioned,the iNOS protein increases obviously while the lung injury is obvious. After the intervention of Dexamethasone，especially in large dose,the iNOS protein declines and the lung injury lessens. [Key