缺血预处理对大鼠心肌细胞凋亡的影响及其机制

The effects of preconditioning on cardiomyocyte apoptosis in rats and the mechanisms

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.