中文摘要：

目的：探讨红景天苷对大鼠局灶性脑缺血-再灌注损伤的保护作用机制与磷脂酰肌醇-3激酶/丝氨酸-苏氨酸蛋白激酶（ PI3-K/AKT）信号通路的相关性。方法将48只SD雄性大鼠按随机数字表法分为四组：假手术组、模型组及红景天苷低、高剂量组。采用线栓法制备右侧大脑中动脉闭塞模型，缺血2 h再灌注24 h后进行神经功能缺损评分及相关指标检测。氯化三苯基四氮唑（ TTC）染色检测脑梗死面积，苏木素-伊红（ HE）染色观察脑组织病理学改变，原位末端标记技术（ TUNEL）法检测细胞凋亡数，免疫组化法检测PI3-K、p-AKT表达。结果与模型组比较，红景天苷高、低剂量组神经功能缺损程度明显减轻，脑梗死体积及凋亡阳性细胞数均明显减少，PI3-K、p-AKT阳性细胞表达明显增加，差异均有统计学意义（ P ＜0.05）；与红景天苷低剂量组相比较，红景天苷高剂量组神经功能缺损程度减轻，脑梗死体积及凋亡阳性细胞数均减少，PI3-K、p-AKT阳性细胞表达增加，差异均有统计学意义（ P ＜0.05）。结论红景天苷通过激活PI3-K/AKT信号通路，从而抑制神经细胞凋亡可能是其对脑缺血-再灌注损伤的保护作用机制之一。

英文摘要：

Objective To explore the mechanism of protective effect of Rhodioloside in cerebral ischemia-reperfusion rats and its relevance to phosphatidylinositol 3-kinases （ PI3-K）/protein serine-threonine kinases （ AKT） signaling pathway .Methods Forty eight Sprague-Dawley rats were randomly divided into four groups： sham-operation group , ischemia-reperfusion group , and Rhodiolo-side treatment groups （5 and 10 mg/kg）.The model of right middle cerebral artery occlusion was established with thread ligation meth -od.The score of the neurological deficit was estimated 2 h followed by 24 h reperfusion.Histopathological changes were observed by hematoxylin-eosin（HE） staining.The infarct volume was measured with triphenyltetrazolium chloride （TTC） staining.Apoptotic cells were assessed with terminal deoxynucleotidyl transferase （TdT）-mediated dUTP nick end labeling （TUNEL） method.The expressions of PI3-K and p-AKT were evaluated with immunohistochemistry .Results The score of the neurological deficit was decreased more ob-viously, the number of apoptotic were decreased more significantly , the expressions of PI3-K and p-AKT were increased more signifi-cantly in the Rhodioloside treatment groups （5 and 10 mg/kg） than in the ischemia-reperfusion group （ P 〈0.05）.The score of the neurological deficit was decreased , the number of apoptotic was decreased , and the expressions of PI 3-K and p-AKT were increased in the Rhodioloside treatment group （10 mg/kg） than the Rhodioloside treatment group （5 mg/kg） （ P 〈0.05）.Conclusions The protective mechanism of Rhodioloside therapy against cerebral ischemia r-eperfusion injury might be associated with activating the PI 3-K/AKT signaling pathway and then inhibiting neuronal apoptosis .