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

Nicha Puangmalai, Wipawan Thangnipon, Rungtip Soi-Ampornkul, Nirut Suwanna, Patoomratana Tuchinda, Saksit Nobsathian

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


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, upregulation of acetylcholinesterase 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 debilitating disease.

Original languageEnglish (US)
Pages (from-to)1492-1498
Number of pages7
JournalNeural Regeneration Research
Issue number9
StatePublished - Sep 2017
Externally publishedYes


  • Acetylcholine
  • Acetylcholinesterase inhibitor
  • Alzheimer’s disease
  • Apoptosis
  • N-benzylcinnamide
  • Natural product
  • Neuronal regeneration
  • Oxidative stress
  • Scopolamine

ASJC Scopus subject areas

  • Developmental Neuroscience


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