目的 观察高血脂大鼠缺血侧大脑皮质额叶内B淋巴细胞瘤-2（Bcl-2）、Bcl-2相关X蛋白（Bax）的表达变化，探讨灯盏乙素对高血脂大鼠脑缺血再灌注损伤的保护作用。 方法 大鼠建立高血脂模型后，线栓法阻塞大脑中动脉建立脑缺血再灌注损伤模型，HE染色观察大脑皮质额叶的病理变化，免疫组织化学和免疫印迹法观察Bcl-2、Bax蛋白的表达变化，同时结合神经行为学评分和2，3，5-氯化三苯基四氮唑（TTC）染色观察大鼠的神经行为及脑梗死灶体积的变化。 结果 与假手术组相比，生理盐水组大鼠脑组织损伤加重，Bcl-2的表达明显减少，Bax的表达明显增高，同时大鼠的神经行为学评分和脑组织梗死灶体积明显增加（P<0.05）。与生理盐水组相比，灯盏乙素治疗组脑组织损伤减轻，Bcl-2的表达明显增多，Bax的表达明显减少，同时大鼠的神经行为学评分和脑组织梗死灶体积明显降低（P<0.05）。 结论 灯盏乙素对高血脂大鼠脑缺血再灌注损伤的保护作用可能是通过促进Bcl-2的表达，抑制Bax的表达实现的。

Objective To investigate the effect of scutellarin after cerebral ischemia-reperfusion injury in rats with hyperlipemia,by observing the expression of B-cell lymphoma-2 (Bcl-2) and Bcl-2 assaciated X protein (Bax) in cerebral cortex with hyperlipemia. Methods After the rat model of hyperlipidemia was established, the focal cerebral ischemia-reperfusion model in hyperlipemia rats was established with thread embolism of the middle cerebral artery. The neurobehavioral score was used to observe the symptoms of neurobehavioral injury. 2,3,5 -triphenyl tetrazolium chloride (TTC）staining was used to observe the cerebral infarct volume. HE staining was used to observe the pathological changes of brain tissue. Immunohistochemistry and Western blotting were used to observe the expressions of Bcl-2 and Bax. Results Compared with the sham-operation group, the neurobehavioral scores,cerebral infarction volum and pathologic damage were significantly increased,the expressions of Bcl-2 was significantly lower, the expressions of Bax was significantly increased in ischemiareperfusion group(P<0.05). Compared with the saline group, the neurobehavioral scores, cerebral infarction volum and pathologic damage were significantly decreased,the expression of Bcl-2 was significantly increased, the expression of Bax was significantly decreased in scutellarin treatment group (P<0.05). Conclusion In cerebral ischemia-reperfusion injury rats with hyperlipemia, scutellarin can alleviate cerebral ischemia-reperfusion injury by promoting the expression of Bcl-2 and inhibiting the expression of Bax.