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Toxicol Appl Pharmacol. 2017 Jan 1;314:48-54. doi: 10.1016/j.taap.2016.11.008. Epub 2016 Nov 18.

A silk peptide fraction restores cognitive function in AF64A-induced Alzheimer disease model rats by increasing expression of choline acetyltransferase gene.

Author information

1
College of Veterinary Medicine, Veterinary Medical Center, Chungbuk National University, Cheongju, Republic of Korea.
2
Department of Food Science and Technology, Chungbuk National University, Cheongju, Republic of Korea.
3
Division of Marine Molecular Biotechnology, Gangneung-Wonju National University, Gangneung, Republic of Korea.
4
Worldway Co., Ltd., Sejong, Republic of Korea.
5
Department of Food Science and Technology, Chungbuk National University, Cheongju, Republic of Korea. Electronic address: hsjeong@cbu.ac.kr.
6
College of Veterinary Medicine, Veterinary Medical Center, Chungbuk National University, Cheongju, Republic of Korea. Electronic address: solar93@cbu.ac.kr.

Abstract

This study investigated the effects of a silk peptide fraction obtained by incubating silk proteins with Protease N and Neutrase (SP-NN) on cognitive dysfunction of Alzheimer disease model rats. In order to elucidate underlying mechanisms, the effect of SP-NN on the expression of choline acetyltransferase (ChAT) mRNA was assessed in F3.ChAT neural stem cells and Neuro2a neuroblastoma cells; active amino acid sequence was identified using HPLC-MS. The expression of ChAT mRNA in F3.ChAT cells increased by 3.79-fold of the control level by treatment with SP-NN fraction. The active peptide in SP-NN was identified as tyrosine-glycine with 238.1 of molecular weight. Male rats were orally administered with SP-NN (50 or 300mg/kg) and challenged with a cholinotoxin AF64A. As a result of brain injury and decreased brain acetylcholine level, AF64A induced astrocytic activation, resulting in impairment of learning and memory function. Treatment with SP-NN exerted recovering activities on acetylcholine depletion and brain injury, as well as cognitive deficit induced by AF64A. The results indicate that, in addition to a neuroprotective activity, the SP-NN preparation restores cognitive function of Alzheimer disease model rats by increasing the release of acetylcholine.

KEYWORDS:

Acetylcholine; Alzheimer disease; Choline acetyltransferase; Cognitive function; Silk peptide

PMID:
27871887
DOI:
10.1016/j.taap.2016.11.008
[Indexed for MEDLINE]

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