Elucidation of the mechanism of delayed neuronal death after global cerebral ischemia by antisense oligodeoxynucleotide of Bax mRNA

摘要为了阐明全脑缺血后迟发性神经元死亡的机制，我们用反义寡核苷酸(反义寡核苷酸)阻断Bax的翻译，研究了Bax的表达和神经保护作用。采用双血管结扎法低血压诱导大鼠流涎。用免疫组织化学方法检测输液后2天Bax蛋白的表达。对脑缺血后7d大鼠海马CA1区存活神经元进行计数，观察其神经保护作用。与正义组或载体组相比，反义组BAT的表达没有显著降低。但与正义组和载体组相比，反义组大鼠海马区CA1区的细胞死亡有减少的趋势。这些发现为支持细胞凋亡在迟发性神经元死亡中的作用提供了证据。我们需要进一步的研究来了解继发于缺血的神经细胞死亡的确切分子机制。

AbstractTo elucidate the mechanism of delayed neuronal death after global ischemia, we studied the expression of Bax and neuroprotoction using antisense oligodeoxynucleotide (antisense) designed to block translation of Bax mRNA.Antisense was infused into left lateral ventricle. lachemia was induced by the two-vessel occlusion method with hypotensiora. Bax expression was studied by immunohistochemistry at 2 days after infusion. Neuroprotection was studied counting surviving neurons in the hippocampus CA1 at 7 days after ischemia. Bat expreBsion was not significantly decreased in the antisense group compared to the sense or vehicle groups. But cell death in the hippocampus CA1 was showing a tendency to decrease in the antisense group compared with the sense or vehicle groups. These findings provide evidence to support the role of apoptosis in delayed neuronal death. We need further study to know exact molecular mechanisms of neuronal cell death secondary to ischemia.