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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 To investigate the protective effect of nalmefene hydrochloride on lung ischemia-reperfusion injury and its mechanism. Methods Fifty rats were randomly divided into model group, high and low dose nalmefene group, dexamethasone group and sham operation group, with 5 rats in each group. In the model group, the model of lung ischemia-reperfusion was successfully established by blocking the left hilar 45 min before releasing the block. The nalmefene (20μg / kg, 10μg / kg) and dexamethasone (5 mg / kg) were injected into tail vein of high and low dose nalmefene group and dexamethasone group respectively 10 minutes before blocking the left hilar. Sham operation group did not deal with. After 60 min of reperfusion, the rats in each group were sacrificed and the left upper lobe tissue was taken for further examination. Results Compared with model group, the lung injury, wet / dry weight ratio, MDA content, β-endorphin, μ receptor and κ receptor in high and low dose nalmefene group and dexamethasone group were significantly decreased (P <0.05 or P <0.01), SOD activity increased significantly (P <0.05 or P <0.01). Compared with the dexamethasone group, the lung injury, the ratio of wet / dry weight, the content of MDA, the content of β-endorphin and μ receptor in the low-dose nalmefene group were significantly decreased (P <0.05) No significant change (P> 0.05), SOD activity was significantly increased (P <0.05). Compared with the low dose nalmefene group, the lung injury, the ratio of wet / dry weight, the content of MDA, the content of β-endorphin, μ receptor and κ receptor in high dose group were significantly decreased (P <0.05) Activity was significantly increased (P <0.05). Conclusion Nalmefene hydrochloride can prevent lung ischemia-reperfusion injury by reducing the expression of β-endorphin, inhibiting the expression of μ receptor and κ receptor and alleviating the oxidative stress in lung tissue.