The molecular and electrophysiological mechanism of Buyanghuanwu Decoction in learning and memory ability of vascular dementia rats

被引:43
作者
Tang, Jinglong [1 ]
Gao, Weijuan [1 ]
Li, Jun [1 ]
Qian, Tao [1 ]
Zhang, Hongbo [1 ]
Liu, Shasha [1 ]
机构
[1] Chengde Med Coll, Dept Pathophysiol, Chengde 067000, Hebei, Peoples R China
基金
中国国家自然科学基金;
关键词
Buyanghuanwu Decoction; Hippocampus CA1 region; ERK2 and CaMKII beta; LTP; Learning and memory; Rats; CAMKII; ISCHEMIA; TRANSCRIPTION; HIPPOCAMPUS; INHIBITION; PLASTICITY; DEATH;
D O I
10.1016/j.brainresbull.2013.09.002
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Buyanghuanwu Decoction (BYHWD), as a traditional Chinese medicine, has been developed to treat vascular dementia for hundreds of years, but the underlying mechanisms remain unknown. In this research, the protective effects of BYHWD on hippocampal neuron were examined in the rats of ischemia-reperfusion. Ischemia-reperfusion injury was induced by the four-vessel occlusion method and continued for 30 days. BYHWD (per 6.25 g/kg/d) was orally given to rats twice each day for 30 days after ischemia-reperfusion, Nimodipine (per 10 mg/kg/d) was orally given to rats twice each day for 30 days. In VD + BYHWD group rats, the neuronal injury in the hippocampal CA1 region was significantly less than that of VD group's. BYHWD of intragastric administration also markedly increased the expression of Extracellular signal-regulated kinase 2 (ERK2) and Calcium/calmodulin-dependent protein kinaseII (CaMKII beta)in the CA1 region. Our results suggested that increased ERK2 and CaMKII beta due to BYHWD may partially account for its effect of neuroprotection standing against ischemic injury in the hippocampal CA1 region, and participated in the rebuilding of synapse, strengthened the expression of LTP, promoted the ability recover of learning and memory in VD rats. (C) 2013 Elsevier Inc. All rights reserved.
引用
收藏
页码:13 / 18
页数:6
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