目的  探讨毛蕊异黄酮对脑缺血/再灌注损伤的影响及其作用机制。   方法  将SPF级雄性SD大鼠40只随机分为假手术组（sham）、模型组（model）、毛蕊异黄酮组（calycosin, 20 mg/kg）和尼莫地平组（nimodipine, 0.7 mg/kg，阳性对照药组），采用改良线栓法建立大鼠大脑中动脉闭塞模型，在体模拟脑缺血/再灌注损伤环境。Zea Longa评分法检测脑缺血/再灌注大鼠神经功能缺损情况；盐酸2,3,5-三苯基四氮（TTC）染色检测脑梗死体积；HE染色检测神经细胞病理形态学改变；尼氏染色观察尼氏小体变化；TUNEL染色检测神经细胞凋亡情况；Western blotting检测凋亡关键蛋白细胞色素 C（Cyt C）、凋亡酶激活因子 1(Apaf-1）、Caspase-9和Caspase-3的表达。   结果  与sham组相比，model组神经功能缺损症状明显（P<0.05），脑梗死体积明显增大（P<0.05），倒置光学显微镜下观察发现神经细胞出现胞体收缩，胞核深染、固缩，细胞生长状态较差，尼氏小体明显减少或消失（P<0.05），凋亡神经细胞明显增多（P<0.05），凋亡关键蛋白Cyt C、Apaf-1、Caspase-9和Caspase-3表达均明显升高（P<0.05）；与model组相比，calycosin 组和nimodipine 组大鼠神经功能缺损症状明显减轻（P<0.05），脑梗死体积明显缩小（P<0.05），光学显微镜下观察发现，神经细胞损伤明显减轻，尼氏小体表达明显增多（P<0.05），凋亡神经细胞明显减少（P<0.05），凋亡关键蛋白Cyt C、Apaf-1、Caspase-9和Caspase-3的表达明显降低（P<0.05）。   结论  毛蕊异黄酮可明显抑制神经细胞凋亡，减轻脑缺血/再灌注损伤，其作用机制与毛蕊异黄酮有效调控Cyt C/Apaf-1凋亡信号通路相关。

Objective  To investigate the effect of calycosin on cerebral ischemia/reperfusion injury and its mechanism.    Methods  Forty SPF male SD rats were randomly divided into sham group, model group, calycosin group (20 mg/kg), nimodipine group (0.7 mg/kg, positive control group). The occlusion model of middle cerebral artery in rats was established by modified thread occlusion method,and the environment of cerebral ischemiareperfusion injury was simulated in vivo. Zea longa score was used to detect the neurological deficit of rats after ischemiareperfusion injury, 2,3,5-triphenyltetranitrogen (TTC) was used to detect the volume of cerebral infarction, HE staining was used to detect the pathomorphological changes of nerve cells, Nissl staining was used to observe the changes of nissl bodies, TUNEL staining was used to detect the apoptosis of nerve cells, Western blotting was used to detect the expression of cytochrome C (Cyt C), apoptotic protease activating factor-1 (Apaf-1), Caspase-9 and Caspase-3.    Results  Compared with the sham group, the neurological deficit symptoms in the model group were significant (P<0.05), the volume of cerebral infarction increased significantly (P<0.05). Under the microscope, it was found that the nerve cells showed contraction of cell body, hyperchromatic and pyknosis of nucleus and poor growth state, the expression of nissl body reduced significantly (P<0.05), the apoptotic nerve increased significantly (P<0.05), the expression of Cyt C, Apaf-1, Caspase-9 and Caspase-3 increased significantly (P<0.05).Compared with the model group, the neurological deficit symptoms of calycosin group and nimodipine group reduced significantly (P<0.05), the volume of cerebral infarction reduced significantly (P<0.05). Under the microscope, the damage of nerve cells reduced significantly , the expression of nissl body increased significantly (P<0.05), the apoptotic nerve reduced significantly (P<0.05), the expression of Cyt C, Apaf-1, Caspase-9 and Caspase-3 decreased significantly (P<0.05)   Conclusion  Calycosin can significantly inhibit the apoptosis of nerve cells and reduce the cerebral ischemia-reperfusion injury. Its mechanism of action is related to the effective regulation of Cyt C/Apaf-1 apoptosis signaling pathway by calycosin.