The fruit of Crataegus pinnatifida ameliorates memory deficits in β-amyloid protein-induced Alzheimer's disease mouse model

被引:24
|
作者
Lee, Jihye [1 ]
Cho, Eunbi [2 ]
Kwon, Huiyoung [2 ]
Jeon, Jieun [2 ]
Jung, Chul Jong [3 ]
Moon, Minho [4 ]
Jeon, Mira [5 ,6 ]
Lee, Young Choon [2 ,6 ]
Kim, Dong Hyun [2 ,6 ]
Jung, Ji Wook [7 ]
机构
[1] Kyungpook Natl Univ, Sch Med, Div Endocrinol, Daegu 41944, South Korea
[2] Dong A Univ, Coll Hlth Sci, Dept Med Biotechnol, Busan 49315, South Korea
[3] Okchundang Corp, 142 Yulam Ro, Daegu, South Korea
[4] Konyang Univ, Coll Med, Dept Biochem, Daejeon 35365, South Korea
[5] Dong A Univ, Coll Hlth Sci, Dept Food Sci & Nutr, Busan 49315, South Korea
[6] Dong A Univ, Inst Convergence Biohlth, Busan 49315, South Korea
[7] Daegu Haany Univ, Coll Bioind, Div Biotechnol & Convergence, Kyungsan 38578, South Korea
关键词
The fruit of Crataegus pinnatifida bunge; Alzheimer's disease; Amyloid beta aggregation; Neuroinflammation; ACTIVATION; OLIGOMERS;
D O I
10.1016/j.jep.2019.112107
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: The fruit of Crataegus pinnatifida is a traditional medicine widely used as digestive drug in East Asia. Although Chinese herbal medicine used it for mental health, scientific evidence does not exist, yet. Aims of study: The aim of this study is to show that the ethanol extract of the fruit of Crataegus pinnatifida (CPE) has neuroprotective effect on Alzheimer' disease model mice. Materials and methods: Intracerebroventricular injection of A beta was used to induce Alzheimer's disease-like pathology. Passive avoidance and Y-maze tasks were used to examine the effect of CPE on memory impairrilents by A beta. Immunohistochemistry was used to examine the effect of CPE on glial activation. ThT assay was used to observe the effect of CPE on A beta aggregation. MTT and LDH release assays were utilized to examine effects of CPE on A beta-induced cytotoxicity. Results: CPE prevented memory deficit in A beta-induced memory impairment model. Moreover, CPE prevented glial activation in the hippocampus of A beta-injected model. In in vitro test, CPE inhibited A beta fibril formation in a concentration-dependent manner. CPE also caused disaggregation of A beta fibrils. Along with this, CPE blocked neuronal cell death induced by A beta. Conclusions: Collectively, these experimental findings demonstrated that CPE could be a candidate for development of AD therapy.
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页数:7
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