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目的研究3-硝基丙酸预处理对大鼠局灶性脑缺血再灌注损伤的作用。方法采用线栓法建立大鼠局灶性脑缺血再灌注损伤模型,将52只大鼠随机分成4组:假手术组、缺血组、3-硝基丙酸预处理组、3-硝基丙酸预处理+5-羟癸酸盐组,并观察各组脑梗死体积和线粒体标志酶活性变化。结果与缺血组比较,3-硝基丙酸预处理组脑梗死体积明显减少[自(22.89±6.97)%减至(9.68±2.05)%],线粒体标志酶活性明显增高,差异具有显著性(P<0.01),而3-硝基丙酸预处理+5-羟癸酸盐组与缺血组比较无明显差异(P>0.01)。结论3-硝基丙酸预处理对大鼠局灶性脑缺血再灌注损伤具有保护作用,其机理与开放线粒体ATP敏感性钾通道、维护线粒体功能和提高其耐受性有关。
Objective To investigate the effect of 3-nitropropionic acid preconditioning on focal cerebral ischemia-reperfusion injury in rats. Methods The model of focal cerebral ischemia-reperfusion injury in rats was established by thread occlusion. Fifty-two rats were randomly divided into 4 groups: sham operation group, ischemia group, 3-nitropropionic acid pretreatment group, Propionic acid + 5-hydroxydecanoate pretreatment group, and observed the changes of cerebral infarction volume and mitochondrial enzyme activity. Results Compared with the ischemic group, the volume of cerebral infarction in 3-nitropropionic acid pretreatment group decreased significantly (from (22.89 ± 6.97)% to (9.68 ± 2.05)%], and the mitochondrial enzyme activity was significantly increased, with significant difference (P <0.01). There was no significant difference between 3-nitropropionic acid pretreatment + 5-hydroxydecanoate group and ischemia group (P> 0.01). Conclusion Pretreatment with 3-nitropropionic acid has a protective effect on focal cerebral ischemia-reperfusion injury in rats. Its mechanism is related to the opening of mitochondrial ATP-sensitive potassium channel, maintaining mitochondrial function and increasing its tolerance.