当归对大鼠局灶性缺血脑组织细胞凋亡的作用

目的 :应用大鼠局灶性脑缺血模型观察当归对脑缺血损伤的治疗作用及其机制。方法 :TTC染色计算脑缺血梗塞灶体积。原位末端标记法观察细胞凋亡并计算凋亡率和凋亡指数。免疫组化观察凋亡相关蛋白Bcl 2及Bax蛋白表达的变化。结果 :①与单纯缺血再灌组相比 ,当归治疗组TTC染色显示当归治疗组脑缺血梗塞区体积缩小 (P <0 .0 5 ) ,凋亡率和凋亡指数较单纯缺血再灌组有明显下降 (P <0 .0 1 ) ,Bcl 2蛋白表达与单纯缺血再灌组无差异 (P >0 .0 5 ) ,而Bax蛋白表达显著减少 (P <0 .0 1 )。②缺血 2h再灌 4 8h组较缺血 2h再灌 2 4h组 ,凋亡细胞明显减少 (P <0 .0 1 )。结论 :①当归能抑制Bax蛋白的表达 ,减少脑缺血区细胞凋亡的发生 ,这是当归治疗大鼠局灶性脑缺血损伤的可能机制之一。②缺血 2h再灌 4 8h ,脑缺血神经细胞迟发性损伤已开始减轻

Effects of Angelica on Apoptosis of Focal Cerebral Ischemic Injury in Rats

Objective: To study the therapeutics and mechanisms of Angelica on the focal cerebral ischemic injury of rats. Methods: The ischemic areas were calculated by TTC stain. And terminal deoxynucleotidyl transferase(TDT) mediated DUTP biotin nick end labeling(TUNEL) method was applied to detect apoptosis. The expressions of Bcl 2 and Bax proteins were observed by immunohistochemical staining methods. Results: ① In the treatment groups with angelica,the volume of cerebral infarction reduced(P<0.05),apoptosis cells reduced significantly (P<0.01),and the expression of Bax decreased(P<0.01). ② The apoptosis cells in the group of 48 h referfusion decreased obviously compared with the group of 24 h reperfusion. Conclusion: ① Angelica can reduce apoptosis cells by decreasing the expression of Bax protein. This is maybe one of the mechanisms of the therapeutic effect of Angelica on focal cerebral ischemic injury. ②Alleviation of the lated neuron injury begins at 48 h of perfusion.