摘要
目的探讨异丙酚对肝缺血再灌注时TNF-α、IL-1含量的影响及其对肺损伤的保护作用。方法 24只SD大鼠随机分为假手术组(s组,n=8)、缺血再灌注组(I/R组)和异丙酚处理组(P组)。阻断肝门30 min后开放血流,建立大鼠全肝缺血再灌注模型。I/R组与p组分别于肝门阻断前10 min腹腔注射异丙酚50 mg/kg或相应剂量生理盐水,于再灌注1 h取血、处死动物。假手术组不阻断肝门,于上述相应时间点注射生理盐水与取血、处死动物。放免法测定血清TNF-α、IL-1的变化,光镜下观察肺组织形态学改变,同时测定肺组织W/D比值。结果 (1)与s组相比,I/R组血清TNF-αI、L-1含量与肺组织W/D比值均显著增加(P均<0.01)。病理学方面,I/R组肺泡腔完整性破坏,间隔增厚,并可见中性粒细胞浸润。(2)与I/R组相比,P组病理学改变减轻;W/D比值、血清TNF-αI、L-1含量均显著降低(P均<0.05)。结论 TNF-aI、L-1β等细胞因子参与了肝缺血再灌注后肺损伤的发生发展过程,丙泊酚可能通过抑制炎性细胞因子的表达,对大鼠肝I/R后肺损伤发挥有保护作用。
Objective To explore the effects of propofol on tumor necrosis factor-alpha(TNF-α),interleukin-1(IL-1) in rats following hepatic ischemia/reperfusion and the protection of propofol on hepatic ischemia–reperfusion-induced lung injury.Methods 24 rats were randomly divided into 3 groups(n=8 in each group):propofol(P) group,ischemia-reperfusion(I/R) group and sham-operation(S) group.Total hepatic I/R was produced by occlusion of hepatic helium for 30 minutes,and the occlusion was then released for reperfusion.In P and I/R group,propofol(50 mg/kg)or normal saline of the same volume was administered intraperitoneally 10 min before ischemia,the animals were killed at 1h of reperfusion.In S group,the hepatic helium wasn't occluded,normal saline was injected and the animals were killed at corresponding time.The concentration of IL-1,TNF-αin serum was determined,and the lung tissue was taken for determination of W/D ratio and histological examination.Results(1)Compared with that in sham-operation group,the concentration of IL-1,TNF-α,W/D ratio were all significantly increased(P〈0.01).Histological examination revealed that the alveolar architecture was destroyed with interstitial thickening and neutrophil infiltration in total hepatic I/R group.(2)Compared with that in I/R group,the concentration of IL-1,TNF-α,W/D ratio were all significantly decreased(P〈0.05=,and the histological changes was less severe in propofol group.Conclusion Propofol can effectively suppress the production and release of inflammatory cytokines and its protective effect might be mediated by anti-inflammation.
出处
《中国实验诊断学》
北大核心
2010年第7期1002-1004,共3页
Chinese Journal of Laboratory Diagnosis
基金
深圳市科技局课题(200803032)