采用免疫细胞化学法 ,观察体外模拟脑缺血再灌注损伤对原代培养海马神经元凋亡调控基因bcl 2和bax的表达及抗呆Ⅰ号 (由天麻素等中药提取物组成 )的影响。结果发现 ,脑缺血再灌注损伤可引起海马神经元bcl 2表达减少和bax表达增加 ,抗呆Ⅰ号可上调神经元bcl 2的表达和下调bax的表达 ,表明抗呆Ⅰ号能通过调节缺血再灌注损伤神经元凋亡调控基因的表达 ,对缺血再灌注损伤神经细胞起到一定的保护作用。 Immunocytochemistry was used to observe the expression of bcl 2 and bax, the apoptosis-regulatory genes in primary cultured hippocampal neurons, and the effect of anti-dead I (composed of gastrodin extracts, etc.) in simulated cerebral ischemia-reperfusion injury in vitro. The results showed that cerebral ischemia-reperfusion injury can cause decreased expression of bcl 2 and increased bax expression in hippocampal neurons. Anti-deaf I can up-regulate the expression of bcl 2 and down-regulate bax expression, indicating that anti-dead I can be adjusted by The expression of apoptosis-regulating genes in reperfusion injury of neurons plays a protective role in ischemia-reperfusion injury of nerve cells.