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Biol Pharm Bull. 2017;40(12):2096-2104. doi: 10.1248/bpb.b17-00378.

The Seed of Zizyphus jujuba var. spinosa Attenuates Alzheimer's Disease-Associated Hippocampal Synaptic Deficits through BDNF/TrkB Signaling.

Author information

1
Department of Medicinal Biotechnology, College of Health Sciences, Dong-A University.
2
Department of Life and Nanopharmaceutical Science, Kyung Hee University.
3
School of Clinical Sciences, Faculty of Medicine and Dentistry, University of Bristol.
4
Department of Aquatic Biomedical Sciences, School of Marine Biomedical Science, College of Ocean Science, Jeju National University.
5
Department of Herbal Medicinal Pharmacology, College of Herbal Bio-Industry, Daegu Haany University.
6
Institute of Convergence Bio-Health, Dong-A University.
7
Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University.
8
Kyung Hee East-West Pharmaceutical Research Institute, College of Pharmacy, Kyung Hee University.

Abstract

Ziziphus jujuba is a plant, which bears fruits and seeds that are used for medicinal purposes in Traditional oriental medicine. The seed of Zizyphus jujuba var. spinosa (EZJ) has been also traditionally used for psychiatric disorders in Chinese and Korean medicines. Recent findings have indicated that EZJ improves memory impairment, a common symptom of various neurological diseases. However, the effects of EZJ on amyloid β (Aβ) toxicity, which is a main cause of Alzheimer's disease (AD), remain to be elucidated. To illuminate the potential anti-AD effect and mechanism in the mouse hippocampal tissue, we examined the effect of standardized EZJ on Aβ-induced synaptic long-term potentiation (LTP) deficit in the hippocampal tissue. EZJ blocked Aβ-induced LTP deficits in a concentration-dependent manner. Moreover, EZJ increased brain-derived neurotrophic factor (BDNF) level in naïve hippocampal slices. The finding that the blockade of BDNF receptor reduced the effect of EZJ suggests that EZJ ameliorates the Aβ-induced LTP deficit through BDNF/topomyosin receptor kinase B (TrkB) signaling. However, transcription or translation inhibitors failed to block the effect of EZJ, suggesting that BDNF synthesis is not required for the action of EZJ on LTP. Finally, we found that EZJ stimulates plasmin activity. In contrast, plasmin inhibitor blocked the effect of EZJ on the Aβ-induced LTP deficit. Our findings indicate that EZJ ameliorates Aβ-induced LTP deficits through BDNF/TrkB signaling. This phenomenon is induced by a regulatory effect of EZJ on the post-translation modification of BDNF.

KEYWORDS:

Zizyphus jujuba var. spinosa; amyloid β (Aβ); brain-derived neurotrophic factor (BDNF); long-term potentiation; plasmin

PMID:
29199234
DOI:
10.1248/bpb.b17-00378
[Indexed for MEDLINE]
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