大鼠全肝缺血再灌注后肺细胞凋亡及异丙酚对细胞凋亡的影响  

Pneumocyte apoptosis after total hepatic ischemia-reperfusion in rats and the effect of propofol on apoptosis

作　　者：姜春玲[1] 王金兰[2] 咸云淑[1] 刘岩[2] 

机构地区：[1]北京大学深圳医院,广东深圳518036 [2]吉林大学中日联谊医院

出　　处：《中国实验诊断学》2009年第7期875-877,共3页Chinese Journal of Laboratory Diagnosis

基　　金：深圳市科技计划项目(项目编号200803032)

摘　　要：目的探讨大鼠全肝缺血再灌注后肺组织细胞凋亡情况及异丙酚对细胞凋亡的影响。方法24只SD大鼠随机分为3组(n=8),异丙酚组、缺血再灌注组与假手术组。阻断肝门30 min后开放血流,建立大鼠全肝缺血再灌注模型。异丙酚组与缺血再灌注组分别于肝门阻断前10min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处死动物。假手术组不阻断肝门,于上述各相应时间点注射生理盐水与处死动物。留取肺脏组织,原位末端转移酶(TUNEL)法检测细胞凋亡,同时检测肺组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、湿/干重(W/D)比值及肺组织病理。结果(1)与假手术组相比,缺血再灌注组W/D比值、AI与MDA含量均显著增高(P均<0.01);SOD活性显著降低(P<0.01);病理学方面,缺血再灌注组肺泡腔完整性破坏,间隔增厚,并可见中性粒细胞浸润。(2)与缺血再灌注组相比,异丙酚组W/D比值、细胞凋亡指数(AI)与MDA含量显著降低(P均<0.01);而SOD活性显著增加(P<0.01);病理学改变减轻。结论细胞凋亡可能在全肝缺血再灌注肺损伤发生过程中具有重要意义;异丙酚对全肝缺血再灌注后肺细胞凋亡具有抑制作用,其作用机制可能与清除自由基、抑制脂质过氧化有关。Objective To explore pneumocyte apoptosis induced by total hepatic ischemia-reperfusion（I/R） in rats and the effect of propofot on cell apoptosis and its related mechanism.Methods 24 rats were randomly divided into 3 groups （ n = 8 in each group） ：prepofol group, I/R group and sham-operation group. Total hepatic I/R was produced by occlusion of hepatic helium for 30 minutes, and the occlusion was then released for reperfusion. In propofol group and I/R group, propofol（50 mg/kg）or normal saline of the same volume was administered intraperitoneally 10 min before isehemia, the animals were killed at lh of repeffusion. In sham-operation group, the hepatic helium wasn＇ t occluded, normal saline was injected and the animals were killed at corresponding time. Then the lung tissue was taken for determation of W/D ratio, MDA content, SOD activity, apoptotic cells, and histolngical examination. Resuits （1）Compared with that in sham-operation group, the W/D ratio, apoptotic index and MDA content were all significantly increased （ P 〈 0.01 ）, and the SOD activity was significantly decreased （P 〈 0.01 ）. Histological examination revealed that the alveolar ;,architecture was destroyed with interstitial thickening and neutrophil infiltration in I/R group. （2）Compared with that in I/R group, the .W/D ratio, apoptotie index and MDA content were all significantly decreased （ P 〈 0.01 ）, and the SOD activity was significantly increased （ P 〈 0.01 ） in propofol group, and the histological changes was less severe. Conclusion Cell apeptosis may play an important role during the development of lung injury induced by total hepatic I/R. Propofol can inhibite pneumocyte apoptosis induced by total hepatic L/R, which might be mediated by anti-oxidation.

关 键 词：异丙酚 细胞凋亡 丙二醛 超氧化物歧化酶 

分 类 号：R96[医药卫生—药理学]