大鼠肺缺血再灌注损伤引起肺细胞的凋亡  

Pulmonary apoptosis induced by ischemia-reperfusion lung injury in rats

作　　者：谢东甫[1] 秦雄[2] 徐志飞[2] 

机构地区：[1]第二军医大学基础医学部细胞生物学教研室,上海200433 [2]长征医院胸心外科,上海200003

出　　处：《第二军医大学学报》2004年第3期295-297,共3页Academic Journal of Second Military Medical University

基　　金：上海市科学技术发展基金 (0 2 4 4 1 90 76)

摘　　要：目的 :观察肺缺血再灌注损伤对肺细胞凋亡的影响。 方法 :雄性 SD大鼠 4 0只 ,体质量 30 0～ 35 0 g,随机分为 8组(缺血再灌注 6组 ,单纯缺血组 ,对照组 ) ,每组 5只。通过阻断肺门建立大鼠原位肺缺血再灌注模型 ,应用末端脱氧核苷酸转移酶 (Td T)介导的 d U TP缺口末端标记技术 (TU NEL)检测缺血再灌注损伤所引起的肺细胞凋亡的变化及其与再灌注时间的相关性 ;DNA电泳进行肺组织细胞 DNA片段分析 ;电镜观察凋亡细胞的超微结构。结果 :在肺缺血再灌注后早期 (30 min)发生明显的肺细胞凋亡 ,凋亡细胞数峰值位于再灌注后 2 h,再灌注后 1 2 h凋亡细胞数与对照组无显著差别 ;缺血而无再灌注的肺细胞凋亡无明显变化。 结论Objective:To observe the pulmonary apoptosis resulted from ischemia reperfusion lung injury in rats. Methods: Forty male SD rats, weighing 300 350 g,were randomly divided into 8 groups: 6 ischemia reperfusion group,simple ischemia group and control group( n =5).An in situ ischemia reperfusion lung injury rat model was established. Apoptotic cells were detected by the terminal deoxynucleotidyl transferase mediate dUTP nick end labelling (TUNEL) technique and the apoptotic DNA fragments by pulmonary DNA electrophoresis. Electron microscopy was performed to verify the morphologic changes of apoptosis. Results: Obvious apoptosis of pneumocytes occurred early after(30 min) ischemia reperfusion lung injury, with the peak on 2 h after reperfusion, and there were no significant differences 12 h after reperfusion compared with control group. There was a slight but no statistically significant elevation of apoptotic pneumocytes number in simple ischemia group compared with controls. Conclusion: The result indicates that apoptosis may contribute significantly to ischemia reperfusion lung injury.

关 键 词：大鼠 肺缺血 再灌注损伤 肺细胞 细胞凋亡 

分 类 号：R655.3[医药卫生—外科学]