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

作者：Cha Yeseul; Lee Sang Hoon; Jang Su Kil; Guo Haiyu; Ban Young Hwan; Park Dongsun; Jang Gwi Yeong; Yeon Sungho; Lee Jeong Yong; Choi Ehn Kyoung; Joo Seong Soo; Jeong Heon Sang^*; Kim Yun Bae^*

来源：Toxicology and Applied Pharmacology, 2017, 314: 48-54.

DOI：10.1016/j.taap.2016.11.008

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

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 300 mg/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.

• 出版日期2017-1-1