Effect of nalmefene hydrochloride on the expressions of pulmonary β-endorphin and IL-8 in rats with lung ischemia -reperfusion injury

YANG Min; XU Biao; ZENG Kun

doi:10.3969/j.issn.1002-1949.2016.06.018

Abstract：Objective To study the inhibition of nalmefene hydrochloride on lung ischemia-reperfusion injury and its mechanism. Methods Fifty rats were randomly divided into model group, high dose of nalmefene group, low dose nalmefene group, dexamethasone group and sham operation group equally( n = 10 ) . The lung ischemia - reperfusion model was established by occlusion of the left pulmonary hilum in the model group. The intravenous injection of nalmefene (20μg/kg, 10μg/kg) and dexamethasone (5 mg/kg) was applied when the model was established in the high dose of nalmefene group, the low dose of nalmefene group and the dexamethasone group respectively. The sham operation group without occlusion of the left pulmonary hilum was not given any treatment. At 6 h after reperfusion, all rats were detected arterial blood gas value and then sacrificed. The specimens from the upper lobe of the left lung tissue were preserved to observe pulmonary lesions, detect the ratio of wet /dry weight and the expressions of MDA, SOD, β - endorphin and IL -8 in lung tissue. Results Compared with the model group, the value of PCO2 , the degree of pulmonary lesions, the ratio of wet /dry weight and the expressions of MDA, β - endorphin and IL -8 in lung tissue were significantly decreased (P< 0. 05 or P< 0. 01), but the value of PO2 and the expression of SOD was significantly increased (P< 0. 05 or P< 0. 01) in the high or low dose nalmefene group and the dexamethasone group. Compared with dexamethasone group, the value of PCO2 , the degree of pulmonary lesions, the ratio of wet / dry weight and the expressions of MDA, β -endorphin and IL -8 in lung tissue were significantly decreased (P < 0. 05), the value of PO2 and the expression of SOD was significantly increased (P< 0. 05), but the expression of IL -8 was not significantly changed in the low dose nalmefene group(P>0. 05). Compared with the low dose of nalmefene group, the value of PCO2, the degree of pulmonary lesions, the ratio of wet / dry weight and the expressions of MDA, β-endorphin and IL-8 in lung tissue were significantly decreased (P < 0. 05), but the value of PO2 and the expression of SOD was significantly increased in the high dose nalmefene group(P< 0. 05). Conclusion Nalmefene hydrochloride may inhibit lung ischemia-reperfusion injury and the effect may depend on its dose. One of the mechanisms is that nalmefene may depress the production of β -endorphin and reduce the degree of oxidative stress and inflammatory reaction in lung tissue.