摘要
目的 观察心肌细胞凋亡及其机制在大鼠心肌缺血再灌注损伤和缺血预处理中的作用.方法 将40只大鼠随机分成4组：对照组（A组）、60min缺血再灌注组（B组）、120min缺血再灌注组（C组）、缺血预适应组（D组）;应用TUNEL法检测心肌组织的凋亡;心脏病理改变用光学和电子显微镜观察;检测肿瘤坏死因子（TNF）-α、bcl-2和bax因子.结果 D组心肌细胞凋亡指数（11.36±4.23）%明显优于B组（18.14±7.69）%和C组（15.59±6.31）%,D组TNF-α、bel-2和bax的表达也明显优于B、C二组.结论 缺血预处理可减轻大鼠心肌缺血再灌注后心肌细胞的凋亡;TNF-α、bcl-2和bax表达的抑制与缺血预处理保护机制有关.
Objective To observe the possible roles of apoptosis and its mechanisms in myocardial ischemia-reperfusion injury and preconditioning protection in rats. Methods Forty rats were randomly divided into four groups ： control group （group A）, 60 min ischemia-reperfusion group （group B）, 120 min ischemia-reperfusion group （group C）, and ischemic-preconditioning group （group D）. Apoptosis was treasured by using terminal deoxynucleotidyl transferase mediated dUTP biotin nick end labelling （TUNEL）. The pathological changes of the heart were observed under the light and and electron microscopies. The expression of tumor necrosis factor （TNF）-α, bcl-2, and bax was detected. Results Apoptosis index and the expression of TNF-α, bcl-2, and bax in group D were significantly lower than those in the group B and group C. Conclusion Ischemic-preconditioning can relieve the apoptosis of myocardial ischemia-reperfu-sion. Inhibiting the expression of TNF-α, bcl-2, and bax accounts for the mechanisms of preconditioning protection.
出处
《中华实验外科杂志》
CAS
CSCD
北大核心
2010年第2期237-238,F0004,共3页
Chinese Journal of Experimental Surgery
基金
浙江省医药卫生科研基金计划资助项目（2007A182）
关键词
心肌
缺血预处理
再灌注损伤
脱噬作用
免疫组织化学
Myocardium
Isehemia preconditioning
Reperfusion injury
Apoptosis
Immunohistochemistry
