Zheng Yong-Qiu, Liu Jian-Xun, Xu Li, Yao Ming-Jiang, Song Wen-Ting
Xiyuan Hospital of China Academy of Chinese Medical Sciences, Beijing 100091, China.
Zhongguo Zhong Yao Za Zhi. 2013 Jul;38(13):2182-6.
To observe the protective effect of the Weinaokang (WNK) and its active compound bilobalide on focal cerebral ischemia reperfusion, and their mechanisms.
The 60-minute middle cerebral artery occlusion (MCAO) was adopted to establish the 24 h-14 d reperfusion model. The expression of Beclin-1 was detected by the Western blotting technique. The transmission electron microscopy was used to observe ultrastructural changes. Neurogenesis was detected by the immunofluorescence staining.
WNK (20, 10 mg x kg(-1), ig) or its active compound bilobalide (10, 5 mg x kg(-1), ig) could promote the generation of mature neurons (BrdU(+) -MAP-2+) at the ischemic side, and inhibit expression of autophagy-related gene Beclin-1, so as to reduce the neuron injury induced by focal cerebral ischemia reperfusion.
WNK and its active compound bilobalide can inhibit neuron autophagy and improve neurogenesis in ischemic peripheral area, suggesting that neurogenesis may be the intervention target for WNK to promote self-repairing of ischemic area.
观察维脑康（WNK）及其活性成分白果内酯对局灶性脑缺血再灌注损伤的保护作用及其机制。
采用大脑中动脉闭塞60分钟法建立24小时至14天再灌注模型。采用蛋白质印迹技术检测Beclin-1的表达。用透射电子显微镜观察超微结构变化。通过免疫荧光染色检测神经发生情况。
WNK（20、10毫克/千克，灌胃）或其活性成分白果内酯（10、5毫克/千克，灌胃）可促进缺血侧成熟神经元（BrdU(+) -MAP-2+）的生成，并抑制自噬相关基因Beclin-1的表达，从而减轻局灶性脑缺血再灌注诱导的神经元损伤。
WNK及其活性成分白果内酯可抑制神经元自噬并改善缺血周边区域的神经发生，提示神经发生可能是WNK促进缺血区域自我修复的干预靶点。
