大鼠大脑中动脉缺血/再灌注模型中Caspase-3的表达

目的 研究Caspase-3在缺血性脑损伤中的作用，进一步探讨缺血性脑血管病的分子机制。方法 用Belayev改良的Longa线栓法制备大鼠局灶性大脑中动脉(MCA)缺血／再灌注模型，TTC染色观察梗死灶的形成，分别用原位杂交及免疫组化技术检测鼠脑中Caspase-3 mRNA与活性蛋白的表达。结果 缺血2小时再灌注24小时，TTC染色见明显的梗死灶形成，正常脑组织、假手术组及MCAO缺血对侧脑中有少量的Caspase-3 mRNA表达，但活性蛋白几无表达；再灌注24小时后，缺血侧脑中Caspase-3 mRNA表达明显增强，蛋白质活化增多，再灌注48小时进一步增加。结论 细胞凋亡机制参与了缺血后迟发性神经元死亡，Caspase-3在其中起重要作用。

Caspase-3 expression on MCA ischemia-reperfusion in rat models

Objective To study the role of caspase 3 in ischemic brain damage of rats, and further understand the molecular mechanisms of ischemic cerebral vascular disease.Methods Rat models of the left middle cerebral artery (MCA) occlusion/reperfusion were made using a modification of the intraluminal sature method of Longa established by Belayev, infarct zones were confirmed by 2,3,5 triphenyltetrazolium chloride (TTC) staining, and caspase 3 expression on brain sections at the mRNA and active protein level was detected with in situ hybridization and immunohistochemistry technique, respectively.Results After 2 hours of left MCA ischemia followed by 24 hours of reperfusion, obvious infarct in the MCA dominate regions was confirmed by TTC staining; low levels of caspase 3 mRNA, and fewer of its active protein expression was found in normal brains, sham brains and contralateral brains of MCAO rats; both caspase 3 mRNA and activated protein expression in ipsilateral region were increased after 24 hours of recirculation, and even higher levels were detected at 48 hours of reperfusion.Conclusion Apoptotic mechanism might involve in delayed neuronal death after cerebral ischemia, and caspase 3 might play an important role in ischemic neuronal injury.