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目的:探讨外源性基质金属蛋白酶(matrix metalloproteinase,MMPs)抑制剂强力霉素对肺缺血再灌注损伤炎性反应的影响。方法:建立大鼠肺缺血再灌注模型,测定肺泡灌洗液(bronchoalveolar lavage,BAL)中明胶酶即MMP-2、MMP-9活性,白细胞计数(WBC);肺组织中MMP-2、MMP-9分布及含量,肿瘤坏死因子-α(TNF-α),超氧化物歧化酶(SOD),丙二醛(MDA)含量及病理学改变。结果:肺缺血再灌注后,MMP-2、MMP-9分泌及活性显著提高,BAL中WBC、肺组织TNF-α、MDA显著升高;应用强力霉素后,MMP-2、MMP-9分泌及活性有显著抑制,BAL中WBC、肺组织TNF-α含量显著降低,肺组织病理改变显著减轻。结论:肺缺血再灌注损伤实质是一种炎症损伤,强力霉素主要通过抑制MMPs的分泌及激活,减轻肺缺血再灌注损伤炎性反应程度,达到肺保护作用。
Objective: To investigate the effect of exogenous matrix metalloproteinase (MMPs) inhibitor, doxycycline, on the inflammatory response of lung ischemia-reperfusion injury. Methods: The model of lung ischemia-reperfusion in rats was established. The activities of MMP-2, MMP-9 and WBC in bronchoalveolar lavage fluid (BAL) -9 distribution and content, tumor necrosis factor-α (TNF-α), superoxide dismutase (SOD), malondialdehyde (MDA) content and pathological changes. Results: The secretion and activity of MMP-2 and MMP-9 were significantly increased after lung ischemia-reperfusion, and the levels of TNF-α and MDA in WBC and lung tissue were significantly increased in BAL. The expression of MMP-2 and MMP- Secretion and activity were significantly inhibited, BAL in WBC, lung tissue TNF-α content was significantly reduced pathological changes in lung tissue was significantly reduced. Conclusion: Pulmonary ischemia / reperfusion injury is a kind of inflammatory injury in essence. Doxycycline can protect the lungs by inhibiting the secretion and activation of MMPs and decreasing the inflammatory reaction in lung ischemia-reperfusion injury.