参芎化瘀胶囊通过磷脂酰肌醇激酶／蛋白激酶B信号通路抑制全脑缺血大鼠神经细胞凋亡

Shenxionghuayu capsule inhibits neuronal apoptosis through the PI3-K/Akt signal pathway after global cerebral ischemia reperfusion in rats

目的：探讨参芎化瘀胶囊对大鼠脑缺血／再灌注损伤神经细胞凋亡的影响。方法：雄性SD大鼠被分成假手术组，模型组，参芎化瘀胶囊高、低剂量组，以改良的Pulsineli4血管阻断（4-VO）法制作全脑缺血模型。免疫组织化学法检测海马区磷脂酰肌醇3-激酶（P13-K）、蛋白激酶B（PKB／Akt）的表达。原位缺口末端标记法（TUNEL）检测凋亡细胞。结果：与假手术组比较，模型组中P13-K、Akt表达增高，凋亡神经细胞数量增多；与模型组比较，参芎化瘀胶囊组中P13一K、Akt表达进一步增多，凋亡神经细胞数量减少，上述变化在高剂量参芎化瘀胶囊组更为明显。结论：参芎化瘀胶囊可抑制全脑缺血大鼠神经细胞凋亡，其机制与P13-K／Akt信号通路有关。

Objective： To investigate the effects of Shenxionghuayu capsule on neuronal apoptosis and its underlying mechanism after global cerebral ischemia reperfusion. Methods： Male Sprague-Dawley rats were divided randomly into 4 groups： sham group, model group, low dose of Shenxionghuayu capsule treatment group and high dose of Shenxionghuayu capsule treatment group. Global cerebral ischemia model was performed by improved four-vessel occlusion as described according to the description of Pulsinelli＇s method. The expressions of phosphatidyrlinositol 3-kinase （PI3-K） and serine/threonine kinase （Akt） were measured by immunohistochemistry; The quantities of apoptotic cells was measured by TUNEL method. Results： Compared with the sham group, the PI3-K, Akt expression and the number of neural apoptotic cells were enhanced in the model group ; Compared with the model group, the number of neural apoptotic cells decreased obviously;The PI3-K and Akt expression increased more; The above mentioned changes were more significant in a high dose of the Shenxionghuayu capsule group. Conclusion： Shenxionghuayu capsule could significantly suppress neuronal apoptosis after cerebral ischemia/ reperfusion injury in rats. The mechanism may be related to regulating PI3K/Akt signal transduction pathway.