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目的观察大鼠肺缺血再灌注(LIRI)损伤后肿瘤坏死因子-α(TNF-α)、血小板活化因子(PAF)含量及相关酶学变化,探讨前列腺素E_1预处理对大鼠肺LIRI的保护作用。方法建立原位阻断肺门的大鼠肺缺血再灌注模型,将54只雄性清洁级SD大鼠随机分成假手术组(SO组)、LIRI组(IR组)和前列腺素E_1组(PGE_1组),每组18只。每组均分别在缺血45 min,再灌注1、2h三个时间点处死大鼠,比较三组大鼠不同时间点肺组织病理学改变及肺组织干/湿重(DAN)比值,TNF-α、PAF水平,丙二醛(MDA)浓度及超氧化物歧化酶(SOD)活性表达水平。结果PGE_1组肺组织DAN比值,TNF-α、PAF、MDA浓度及SOD活性水平均较IR组显著改善,差异有统计学意义(P<0.05)。结论前列腺素E_1预处理可以减轻LIRI肺损伤,其可能机制是通过减轻LIRI后的炎症反应而起到肺组织保护作用。
Objective To observe the changes of tumor necrosis factor-α (TNF-α) and platelet-activating factor (PAF) and the related enzymological changes after lung ischemia-reperfusion (LIRI) injury in rats and explore the effect of prostaglandin E_1 preconditioning on lung LIRI Protective effects. Methods Fifty - four male SD rats were randomly divided into sham operation group (SO group), LIRI group (IR group) and prostaglandin E_1 group (PGE_1 group) Group), 18 in each group. Rats in each group were sacrificed at 45 min after ischemia and 1 and 2 h after reperfusion respectively. The lung histopathological changes and lung tissue dry / wet weight (DAN) ratio at different time points were compared. TNF- α, PAF levels, malondialdehyde (MDA) and superoxide dismutase (SOD) activity. Results Compared with IR group, the lung ratios of DAN, TNF-α, PAF, MDA and SOD activity in PGE_1 group were significantly improved (P <0.05). Conclusion Pretreatment with prostaglandin E 1 can attenuate lung injury induced by LIRI. Its possible mechanism is to protect lung tissue by reducing the inflammatory response after LIRI.