盐酸纳美芬对大鼠肺缺血-再灌注损伤的预防作用  

Preventive effect of nalmefene hydrochloride on lung ischemia-reperfusion injury in rats

作　　者：徐标[1] 杨敏[1] 曾昆[1] 

机构地区：[1]华中科技大学同济医学院附属普爱医院(西区),湖北武汉430035

出　　处：《现代预防医学》2016年第14期2617-2620,2627,共5页Modern Preventive Medicine

基　　金：武汉市卫计委科研项目(WX14C58)

摘　　要：目的研究盐酸纳美芬保护肺缺血-再灌注损伤的作用及其机制。方法将50只大鼠随机均分为模型组、高、低剂量纳美芬组、地塞米松组、假手术组共5组,每组10只。模型组采用阻断左肺门45 min后解除阻断成功建立肺缺血-再灌注模型。高、低剂量纳美芬组、地塞米松组分别于阻断左肺门前10 min尾静脉注射纳美芬(20μg/kg、10μg/kg)、地塞米松(5 mg/kg)。假手术组不予处理。于再灌注60 min后处死各组大鼠,留取左肺上叶组织待检。结果与模型组比较,高、低剂量纳美芬组、地塞米松组肺组织损伤程度、湿/干重比值、MDA含量、β-内啡肽、μ受体、κ受体表达均显著降低(P<0.05或P<0.01),SOD活性显著升高(P<0.05或P<0.01)。与地塞米松组比较,低剂量纳美芬组肺组织损伤程度、湿/干重比值、MDA含量、β-内啡肽、μ受体表达均显著降低(P<0.05),κ受体表达无明显变化(P>0.05),SOD活性显著升高(P<0.05)。与低剂量纳美芬组比较,高剂量组肺组织损伤程度、湿/干重比值、MDA含量、β-内啡肽、μ受体、κ受体表达均显著降低(P<0.05),SOD活性显著升高(P<0.05)。结论盐酸纳美芬可通过减少肺组织内β-内啡肽生成、抑制μ受体、κ受体的表达,减轻氧化应激反应而发挥预防肺缺血-再灌注损伤作用。Objective The aim of this study was to investigate the protective effect of nalmefene hydrochlofide on lung ischemia-reperfusion injury and its mechanism. Methods A total of 50 rats were randomly divided into model group, nalmefene high dose group, nalmefene low dose group, dexamethasone group and sham operation group equally （n=10）. The lung ischemia-reperfusion model was established by releasing after occlusion of the left pulmonary hilum for 45 minutes in model group. The intravenous injection of nalmefene （20μg/kg and 10μg/kg） and dexamethasone （5mg/kg） were applied at 10 minutes before occlusion of the left pulmonary hilum in the high and nalmefene low dose group as well as the dexamethasone group. The sham operation group was not disposed. All rats were sacrificed at 60 minutes after reperfusion. The specimens from the upper lobe of the left lung tissue were preserved to observe pulmonary lesions, the ratio of wet/dry weight and the expressions of MDA, SOD, [3-endorphin, ix-receptor and K--receptor in lung tissue were analyzed. Results Compared with the model group, the degree of pulmonary lesions, the ratio of wet/dry weight and the expressions of MDA, β-endorphin, μ- receptor and K-receptor in lung tissue were significantly decreased （P 〈 0.05 or P 〈 0.01）, but the expression of SOD was significantly increased （P 〈 0.05 or P 〈 0.01） in the nalmefene high and low dose group and the dexamethasone group. Compared with dexamethasone group, the degree of pulmonary lesions, the ratio of wet/dry weight and the expressions of MDA, 13-endorphin, tx-receptor in lung tissue were significantly decreased （P 〈 0.05）, the expression of SOD was significantly increased （P 〈 0.05）, but the expression of K-receptor was not significantly changed （P 〉0.05） in the nalmefene low dose group. Compared with the nalmefene low dose group, the degree of pulmonary lesions, the ratio of wet/dry weight and the expressions of MDA, β-endorphin, Ix-receptor and K-receptor in lung tissue we

关 键 词：盐酸纳美芬 肺缺血-再灌注损伤 Β-内啡肽 氧化应激 

分 类 号：R285.5[医药卫生—中药学]