摘要
目的 研究Bcl 2基因转染对小鼠心脏移植再灌注损伤保护作用。方法 采用小鼠颈部异位心脏移植模型 ,BALB/C小鼠 ,随机分为 3组 :假手术组 ,对照组和Bcl 2组。术后 6h测定血清心肌酶谱LDH、GOT、CPK及血清脂质过氧化的终产物MDA、过氧化物歧化酶SOD的含量 ,电镜观察心肌组织的病理变化。TUNEL法染色检测细胞凋亡 ,以心肌凋亡阳性细胞数占总心肌细胞数的百分比作为心肌细胞凋亡指数。结果 Bcl 2组心肌线粒体等结构损伤明显减轻 ,血清心肌酶谱明显改善 (P<0 .0 1) ,MDA明显减少 (P <0 .0 1) ,SOD明显增加 (P <0 .0 1) ,心肌细胞凋亡指数明显降低 (6 .38%± 0 .32 % )比 (42 .4 8%± 2 .34% ) ,P <0 .0 1。结论 Bcl 2基因转染能有效减轻脂质过氧化反应 ,保护心肌线粒体 ,抑制心肌细胞凋亡 ,对心脏移植再灌注损伤有显著保护作用。
Objective To explore the protective effect of Bcl-2 on reperfusion injury in mice heart transplantation. Methods Model of mice cervical heterotopic heart transplantation was set up. In Bcl-2 group, Bcl-2 gene was transfected into isolated donor heart within 1 hour, then that heart was transplanted to the receptor. In control group, heart was directly transplanted to the receptor. Six hours later, levels of lactatedehydrogenase（LDH）, glutamic oxaloacetic transminase（GOT）, creatin phosphokinase（CPK） in sera were detected. Levels of malondialdehyde（MDA） and superoxide dismutase（SOD） in sera were measured by radioimmunoassay acid fluorescence method and radioimmuoassay, respectively. Pathological changes of myocardium especially in mitochodrial integrity were detected by transmission electron microscope. Apoptosis was demonstrated with TUNEL staining. Apoptotic index was evaluated by the percentage of positive cells. Results Levels of LDH , GOT, CPK and MDA in Bcl-2 group was significant lower than those in control group （P 〈0. 01）. Levels of SOD in Bcl-2 group, however, were significant higher than those in control group （P 〈0. 01）. Ultrastructural damage of mycardial cells was significantly alleviated in Bcl-2 group. Apoptotic index of mycardial cells in Bcl-2 group was significant lower than that of control group. Conclusions Bcl-2 has some protective effects on reperfusion injury in mice heart transplantation through getting the lipid oxidation reaction decreased in heart.
出处
《中华小儿外科杂志》
CSCD
北大核心
2005年第1期38-41,共4页
Chinese Journal of Pediatric Surgery
关键词
心脏移植
心肌再灌注损伤
细胞死亡
程序
Heart transplantation
Myocardial reperfusion injury
Apoptosis
