脑脉通对老龄大鼠脑缺血再灌注神经细胞凋亡及相关基因表达的影响

目的　从神经细胞凋亡方面研究脑脉通对老龄大鼠脑缺血再灌注脑损伤的保护作用。方法　采用线栓法建立老龄大鼠急性局灶性脑缺血再灌注损伤模型 ,观察脑脉通对老龄大鼠脑缺血 3h及再灌注 3h、6h、1 2h、2 4h、72h各组神经细胞凋亡及相关的Bcl 2、Bax基因表达影响 ,并与尼莫地平对照。结果　脑缺血再灌注脑组织细胞损伤明显 ,细胞凋亡显著 ,Bax表达增强。脑脉通和尼莫地平能够明显改善脑组织损伤 ,降低神经细胞凋亡。在脑缺血再灌注过程中 ,尼莫地平可使缺血 3h及再灌注 3h的Bcl 2表达增强 ,降低缺血再灌注过程中Bax表达。脑脉通可明显促进Bcl 2表达和降低Bax表达。脑脉通促进Bcl 2表达的作用明显强于尼莫地平。结论　脑脉通可以通过调控细胞凋亡相关基因Bcl 2 /Bax基因表达 ,对局灶性脑缺血 /再灌后神经元起保护作用

Effect of Naomaitong on brain neuron apoptosis and related gene expression in the aged rats with focal cerebral ischemia reperfusion injury

Objective To study the neuro-protective effect of Naomaitong on brain damage after focal cerebral ischemia reperfusion (I/R) in the aged rats. Methods The aged SD rats were subjected to middle cerebral artery occlusion with intraluminal filament technique for 3 hours, followed by reperfusion for 3 h, 6 h, 12 h, 24 h and 72 h, respectively. The effect of Naomaitong on brain cell apoptosis and related apoptosis gene Bcl-2 and Bax expression were monitored with TUNEL and immunohistochemistry, and the group with nimodipine was as control. Results Brain cell apoptosis and issue damage in treated groups (Naomaitong, nimodipine) were decreased compared with the untreated groups. Naomaitong and nimodipine could enhance Bcl-2 expression and decrease Bax expression; therefore they could protect neurons from damages in the ischemia zone. The neuro-protective effect of Naomaitong was as same as that of nimodipine in the early period, but the effect was much better than that of nimodipine in the late stage. Conclusions Naomaitong could protect brain cell from damage after focal cerebral I/R in the aged rats by adjusting Bcl-2 and Bax gene expression.