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目的:探讨卡托普利对脂多糖诱导SD大鼠急性肺损伤的保护作用及可能作用机制。方法:气管滴入LPS的方法制作ALI模型,分别进行肺系数、肺含水量、肺组织病理评分;分光光度计法测定肺组织中SOD、GSH-Px活性及MDA含量;酶联免疫法测定血浆中ICAM-1、TNF-α和IL-1β含量。结果:用卡托普利治疗后,大鼠肺系数、肺含水量及肺组织病理评分显著降低(P<0.05或P<0.01);肺组织的SOD、GSH-Px活性显著升高及MDA含量降低(P<0.05或P<0.01),血浆中ICAM-1、TNF-α和IL-1β含量均显著降低(P<0.05或P<0.01)。结论:卡托普利对脂多糖所致急性肺损伤大鼠具有保护作用,其机制可能与其清除氧自由基、抑制炎症细胞因子的表达有关。
Objective: To investigate the protective effect of captopril on lipopolysaccharide-induced acute lung injury in SD rats and its possible mechanism. Methods: ALI model was established by tracheal instillation of LPS, lung coefficient, lung water content and lung histopathological score were respectively determined. The activities of SOD, GSH-Px and MDA in lung tissue were determined by spectrophotometer. In the ICAM-1, TNF-α and IL-1β content. Results: After treatment with captopril, the lung coefficient, lung water content and lung histopathological score were significantly decreased (P <0.05 or P <0.01); the activities of SOD and GSH-Px in lung tissue were significantly increased and MDA content (P <0.05 or P <0.01). The contents of ICAM-1, TNF-α and IL-1β in plasma decreased significantly (P <0.05 or P <0.01). Conclusion: Captopril has a protective effect on lipopolysaccharide-induced acute lung injury in rats, and its mechanism may be related to scavenging oxygen free radicals and inhibiting the expression of inflammatory cytokines.