Protective effect of β-asarone on AD rat model induced by intracerebroventricular injection of Aβ₁₋₄₂ combined 2-VO and its mechanism.
10.19540/j.cnki.cjcmm.20171218.004
- Author:
Bo-Lin WANG
1
;
Ling XUAN
1
;
Shi-Jie DAI
1
;
Li-Ting JI
1
;
Chang-Yu LI
1
;
Yuan-Xiao YANG
2
Author Information
1. College of Pharmacy, Zhejiang Chinese Medical University, Hangzhou 310053, China.
2. Department of Basic Medicine, Hangzhou Medical College, Hangzhou 310053, China.
- Publication Type:Journal Article
- Keywords:
2-VO;
Alzheimer′s disease;
Aβ₁₋₄₂;
HIF-1α;
antioxidant enzymes;
β-asarone
- From:
China Journal of Chinese Materia Medica
2017;42(24):4847-4854
- CountryChina
- Language:Chinese
-
Abstract:
This study was aimed to investigate the protective effect and mechanism of β-asarone on the animal model of Alzheimer's disease(AD) which was induced by intracerebroventricular injection of Aβ₁₋₄₂ combined cerebral ischemia. One hundred and five rats were randomly divided into seven groups including sham-operated group, AD model group, β-asarone 10 mg•kg⁻¹ group, β-asarone 20 mg•kg⁻¹ group, β-asarone 30 mg•kg⁻¹ group, donepezil group(0.75 mg•kg⁻¹) and Ginkgo biloba extract group(24 mg•kg⁻¹). Rats' learning and memory abilities, cerebric regional blood flow, pathological changes in hippocampal CA1 region, the expression level of HIF-1α and serum CAT, SOD and MDA level were detected 4 weeks later. The results showed that the application of intracerebroventricular injection of Aβ₁₋₄₂ joint 2-VO could lead to rats' dysfunction of learning and memory, decrease in regional cerebral blood flow. Neurons in CA1 region were arranged in disorder, and amyloid deposition was increased. The number of cerebral cortical cells expressing HIF-1α was increased as well. The level of serum CAT and SOD decreased, while level of serum MDA increased. However these symptoms were improved by 20 mg•kg⁻¹ and 30 mg•kg⁻¹ β-asarone. The results indicated that β-asarone could effectively relieve the symptoms of the AD model induced by intracerebroventricular injection of Aβ₁₋₄₂ combined cerebral ischemia, and the potential mechanism might be that it could attenuate damage of MDA to the body by improving the level of CAT and SOD, meanwhile the level of HIF-1α decreased as the decline of hyperoxide which might attenuate its damage to neuron, so it finally achieved alleviating Alzheimer's disease.
