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L-3-n-butylphthalide protects against vascular dementia via activation of the akt kinase pathway

Neural Regeneration Research 2013年第19期8卷 1733-1742页

作者： Yaping Huai Yanhong Dong Jing Xu Nan Meng Chunfeng Song Wenbin Li Peiyuan Lv Department of Neurology Hebei Medical University Department of Neurology Hebei General Hospital Electron Microscope Center Hebei Medical University Department of Pathophysiology Hebei Medical University

As a neuroprotective drug for the treatment of ischemic stroke, 3-n-butylphthalide, a celery seed ex- tract, has been approved by the State Food and Drug Administration of China as a clinical therapeutic drug for ischemic stroke patients. L-3-n-butylphthalide possesses significant efficacy in the treatment of acute ischemic stroke. The activated akt kinase pathway can prevent the death of nerve cells and exhibit neuroprotective effects in the brain after stroke. This study provides the hypothesis that I-3-n- butylphthalide has a certain therapeutic effect on vascular dementia, and its mechanism depends on the activation of the akt kinase pathway. A vascular dementia mouse model was established by cere- bral repetitive ischemia/reperfusion, and intragastrically administered I-3-n-butylphthalide daily for 28 consecutive days after ischemia/repedusion, or 7 consecutive days before ischemia/reperfusion. The Morris water maze test showed significant impairment of spatial learning and memory at 4 weeks after operation, but intragastric administration of I-3-n-butylphthalide, especially pretreatment with I-3-n- butylphthalide, significantly reversed these changes. Thionine staining and western blot analylsis showed that preventive and therapeutic application of I-3-n-butylphthalide can reduce loss of pyrami- dal neurons in the hippocampal CA1 region and alleviate nerve damage in mice with vascular demen- tia. In addition, phosphorylated akt expression in hippocampal tissue increased significantly after I-3-n- butylphthalide treatment. Experimental findings demonstrate that I-3-n-butylphthalide has preventive and therapeutic effects on vascular dementia, and its mechanism may be mediated by upregulation of phosphorylated akt in the hippocampus.

关键词： neural regeneration brain injury ischemia/reperfusion akt phosphorylated akt Morris water maze cog-nitive function 3-n-butylphthalide hippocampus learning memory dementia grants-supported paper neuroregeneration

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