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

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• 作者：Yeseul Cha^a ; ¹ ; Sang Hoon Lee^b ; ¹ ; Su Kil Jang^c ; Haiyu Guo^a ; Young-Hwan Ban^a ; Dongsun Park^a ; Gwi Yeong Jang^b ; Sungho Yeon^b ; Jeong-Yong Lee^d ; Ehn-Kyoung Choi^a ; Seong Soo Joo^c ; Heon-Sang Jeong^b ; ^{hsjeong@cbu.ac.kr} ; Yun-Bae Kim^a ; ^{solar93@cbu.ac.kr}
• 关键词：ACh ; acetylcholine ; AChE ; acetylcholinesterase ; AD ; Alzheimer disease ; BF-7 ; brain factor-7 ; ChAT ; choline acetyltransferase ; CNS ; central nervous system ; CSF ; cerebrospinal fluid ; F3.ChAT ; neural stem cell encoding ChAT gene ; GFAP ; glial fibrillary acidic protein ; MAO-B ; monoamine oxidase-B ; NSC ; neural stem cell ; PD ; Parkinson disease ; SAA ; silk amino acid ; SP-NN ; silk protein degraded by Protease N and Neutrase ; SP-PN ; silk protein degraded by Protease P and Neutrase ; SP ; silk peptide ; SPPS
• 刊名：Toxicology and Applied Pharmacology
• 出版年：2017
• 出版时间：1 January 2017
• 年：2017
• 卷：314
• 期：Complete
• 页码：48-54
• 全文大小：900 K
• 卷排序：314

文摘

Cognition-enhancing effects of SP-NN, a silk peptide preparation, were investigated. SP-NN enhanced ChAT mRNA expression in F3.ChAT neural stem cells and Neuro-2a neuroblastoma cells. Active molecule was identified as a dipeptide composed of tyrosine-glycine. SP-NN reversed cognitive dysfunction elicited by AF64A. Neuroprotection followed by increased acetylcholine level was achieved with SP-NN.