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目的探讨脑缺血时的组织病理学变化及酸敏感离子通道2a(ASIC2a)在缺血预处理诱导的脑缺血模型耐受中的作用。方法取成年雄性SD大鼠160只,随机分为假手术组、预缺血组、缺血组、缺血预处理组共4组。行焦油紫染色观察各组大鼠海马CA1区存活神经元密度,TUNEL染色观察大鼠海马CA1区神经元凋亡情况,RT-PCR和Western blotting检测ASIC2a在大鼠海马CA1区mRNA和蛋白表达情况。结果缺血预处理能够显著减少大鼠海马CA1区锥体神经元的死亡和凋亡,PC+Isch组和Isch组相比具有显著性差异(P<0.01)。全脑缺血能够上调ASIC2a在大鼠海马CA1区mRNA和蛋白表达,在24 h达到高峰,而缺血预处理进一步上调ASIC2a表达,呈进行性上升,在24 h和72 h时相点,PC+Isch组和Isch组相比具有显著性差异(P<0.01)。结论在脑缺血耐受中,缺血预处理对第二次致死性缺血表现出保护作用。在这个过程中,大鼠海马CA1区ASIC2a基因和蛋白表达上调发挥了重要的保护作用。
Objective To investigate the histopathological changes of cerebral ischemia and the role of acid-sensitive ion channel 2a (ASIC2a) in tolerance of ischemic preconditioning-induced cerebral ischemia. Methods 160 adult male Sprague-Dawley rats were randomly divided into 4 groups: sham-operated group, pre-ischemic group, ischemic group and ischemic preconditioning group. The tarry purple staining was used to observe the neuron density of hippocampal CA1 region of rats in each group. TUNEL staining was used to observe the neuronal apoptosis in hippocampal CA1 region. The mRNA and protein expression of ASIC2a in rat hippocampal CA1 region were detected by RT-PCR and Western blotting . Results Ischemic preconditioning could significantly reduce the apoptosis and apoptosis of pyramidal neurons in hippocampal CA1 region of rats. There was a significant difference between PC + Isch group and Isch group (P <0.01). Cerebral ischemia increased ASIC2a mRNA and protein expression in CA1 region of rat hippocampus, reaching a peak at 24 h, while ischemic preconditioning further increased ASIC2a expression, showing a progressive increase at 24 h and 72 h, + Isch group and Isch group compared with a significant difference (P <0.01). Conclusion In ischemic tolerance, ischemic preconditioning has the protective effect on the second lethal ischemia. In this process, ASIC2a gene and protein in rat hippocampus CA1 area play an important role in the protection.