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目的 :探讨布洛芬预防给药防治急性肺损伤 (ALI)的疗效及其可能机制。方法 :用油酸复制ALI大鼠模型。实验分正常对照组、模型组和布洛芬治疗组 ,检测各组肿瘤坏死因子 α(TNF α)浓度、肺湿干比重、肺系数 ,并对肺组织进行病理组织学检查。结果 :布洛芬治疗组在 1.5h时间点血浆TNF α浓度 ( 3 71.0 0± 41.60 pg/ml)较之模型组 ( 73 3 .2 0± 2 48.5 0pg/ml)有显著性降低 (P <0 .0 5 ) ,肺湿干重比、肺系数分别减至 5 .80± 1.0 0和 5 .40± 0 .70 ,肺组织损伤明显减轻。结论 :布洛芬能减少TNF α的产生 ;布洛芬预处理可能是减轻ALI的原因之一。
Objective: To investigate the efficacy and possible mechanism of ibuprofen in prevention and treatment of acute lung injury (ALI). Methods: ALI rat model was replicated with oleic acid. The experimental group was divided into normal control group, model group and ibuprofen treatment group. Tumor necrosis factor α (TNFα) concentration, lung wet-dry proportion and lung coefficient were detected in each group. Pathological examination was also performed on lung tissue. Results: In the ibuprofen treatment group, the plasma TNFα concentration at 3 hours was significantly lower than that of the model group (73.00 ± 41.60 pg / ml) (73.32 ± 0.548 pg / ml) (P < 0. 05), the ratio of wet to dry weight of lung and pulmonary coefficient were decreased to 5.80 ± 1.0 0 and 5.40 ± 0.70, respectively. The lung injury was significantly reduced. Conclusion: Ibuprofen can reduce the production of TNFα; ibuprofen preconditioning may be one of the reasons to reduce ALI.