论文部分内容阅读
采用Ｐｕｌｓｉｎｅｌｉ－Ｂｒｉｅｒｌｅｙ４血管阻塞脑缺血模型观察了大鼠全脑缺血２０ｍｉｎ再灌流８ｈ，ｃ－ｆｏｓ基因表达及再灌流７ｄ海马ＣＡ１区迟发性神经元损害。在缺血再灌流早期（８ｈ）海马ＣＡ１区极少ｃ－ｆｏｓ表达，而齿状回、海马ＣＡ３区、杏仁核大量ｃ－ｆｏｓ表达。缺血再灌流晚期（７ｄ）镀银染色显示海马ＣＡ１区神经元及其突触终末带呈黑色溃变相，而齿状回、海马ＣＡ３区、杏仁核呈金黄色正常相。相邻切片ＨＥ染色示缺血组海马ＣＡ１区核完整的锥体细胞数（５±２．６个／２００μｍ）与对照组（４０±２．９个／μｍ）比较差异有显著意义（Ｐ＜０．０１）。脑缺血诱导的ｃ－ｆｏｓ基因表达对于缺血易损海马ＣＡ１区迟发性神经元坏死可能起直接的调控作用。
The cerebral ischemia model of Pulsineli-Brierley4 occlusion was used to observe the expression of c-fos gene and the delayed neuronal damage of hippocampal CA1 area on the 7th day after reperfusion for 20 minutes in 20 minutes reperfusion. In the early stage of ischemia-reperfusion (8h), c-fos was rarely expressed in the hippocampal CA1 region, while a large number of c-fos was expressed in the dentate gyrus, hippocampal CA3 region and amygdala. Silver staining in the late stage of ischemia reperfusion (7d) showed that the neurons in the CA1 area of the hippocampus and their terminal synaptic terminals showed a black degenerative phase, while the dentate gyrus, the hippocampal CA3 area and the amygdala showed golden yellow normal phase. The number of pyramidal neurons in hippocampal CA1 subfield in ischemic group (5 ± 2.6 / 200μm) was significantly higher than that in control group (40 ± 2.9 / μm) (P < 0.01). Cerebral ischemia-induced c-fos gene expression may play a direct role in the regulation of delayed neuronal necrosis in hippocampal CA1 region.