Neuroprotection of N-benzylcinnamide on scopolamine-induced cholinergic dysfunction in human SH-SY5Y neuroblastoma cells

作     者：Nicha Puangmalai Wipawan Thangnipon Rungtip Soi-ampornkul Nirut Suwanna Patoomratana Tuchinda Saksit Nobsathian 

作者机构：Research Center for Neuroscience Institute of Molecular Biosciences Mahidol University Department of Biochemistry Faculty of Medicine Siriraj Hospital Mahidol University Department of Companion Animal Clinical Sciences Faculty of Veterinary Medicine Kasetsart University Department of Chemistry Faculty of Science Mahidol University Nakhon Sawan Campus Mahidol University 

出 版 物：《Neural Regeneration Research》 (中国神经再生研究（英文版）)

年 卷 期：2017年第12卷第9期

页      面：1492-1498页

核心收录：

学科分类：1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基　　金：supported by a joint Mahidol University and The Thailand Research Fund(TRF)grant(IRG5780009) TRF Royal Golden Jubilee Ph.D.Program(grant No.PHD/0175/2552) the Office of the Higher Education Commission,Ministry of Education,Thailand 

主　　题：Alzheimer's disease acetylcholine apoptosis acetylcholinesterase inhibitor oxidative stress N-benzylcinnamide natural product scopolamine neuronal regeneration 

摘      要：Alzheimer＇s disease, a progressive neurodegenerative disease, affects learning and memory resulting from cholinergic dysfunction. Scopolamine has been employed to induce Alzheimer＇s disease-like pathology in vivo and in vitro through alteration of cholinergic system. N-benzylcinnamide （PT-3）, purified from Piper submultinerve, has been shown to exhibit neuroprotective properties against amyloid-β-induced neuronal toxicity in rat cortical primary cell culture and to improve spatial learning and memory of aged rats through alleviating oxidative stress. We proposed a hypothesis that PT3 has a neuroprotective effect against scopolamine-induced cholinergic dysfunction. PT-3 （125-200 nM） pretreatment was performed in human neuroblastoma SH-SY5Y cell line following scopolamine induction. PT-3 （125-200 nM） inhibited scopolamine （2 mM）-induced generation of reactive oxygen species, cellular apoptosis, upregutation of ace- tylcholinesterase activity, downregulation of choline acetyltransferase level, and activation of p38 and JNK signalling pathways. These findings revealed the underlying mechanisms of scopolamine-induced Alzheimer＇s disease-like cellular dysfunctions, which provide evidence for developing drugs for the treatment of this de- bilitating disease.