脑心通抑制脑缺血诱导的内质网凋亡通路

The Apoptosis Pathway Related with Endoplasmic Reticulum Inhibited by Naoxintong After Focal Cerebral Ischemia

目的观察脑心通对大鼠缺血脑组织内质网凋亡通路caspase-12表达的影响,探讨其对大鼠局灶性脑缺血损伤的保护机制。方法采用线栓法制备大鼠局灶性脑缺血模型。大鼠随机分为假手术组、缺血组以及缺血后脑心通治疗组(n=30),应用组织学观察、免疫组织化学方法及半定量RT-PCR检测缺血不同时段caspase-12表达变化。结果脑缺血6 h caspase-12转录表达增加,12 h达高峰,24h下降。脑心通治疗组与缺血组同时间在相同脑区比较caspase-12转录表达明显减少。假手术组caspase-12无表达。结论脑心通可抑制脑缺血所致的caspase-12凋亡通路,减轻脑缺血造成的损害。

Objective To investigate effect of Naoxintong on focal cerebral ischemia of rats through observing the expression of the caspase-12 related with endoplasmic reticulum.Methods Focal transient cerebral ischemia model of rats was established with intraluminal occlusion of left middle cerebral artery（MCAO）.The rats were randomly divided into sham operated group,ischemic group and Naoxintong treatment group（n=30）.Immunocyto-chemistry and RT-PCR techniques were used to assess the expression of caspase-12 at 6h,12h and 24h respectively after middle artery occlusion of the rats. Results The expressions of caspase-12 mRNA were lower in Naoxintong group compared with the MCA group at 6h and higher at 12h after cerebral ischemia and the expressions at 24h decreased significantly.There were no significant expression in sham group.Conclusion Naoxintong inhibited the expressions caspase-12 in ischemic areas and reduced the damage of neurons after ischemia.