N-benzylcinnamide protects rat cultured cortical neurons from β-amyloid peptide-induced neurotoxicity

Wipawan Thangnipon, Nicha Puangmalai, Vorapin Chinchalongporn, Chanati Jantrachotechatchawan, Narisorn Kitiyanant, Rungtip Soi-ampornkul, Patoomratana Tuchinda, Saksit Nobsathian

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

The pathogenesis of Alzheimer's disease involves an amyloid β-peptide (Aβ)-induced cascade of elevated oxidative damage and inflammation. The present study investigates the protective effects and the underlying mechanisms of N-benzylcinnamide (PT-3), purified from Piper submultinerve. Against Aβ-induced oxidative stress and inflammation in rat primary cortical cell cultures. Pre-treatment with 10-00nM PT-3 significantly attenuated neuronal cell death induced by 10μM Aβ1-42. PT-3 was found to enhance cell viability through a significant reduction in the level of reactive oxygen species, down-regulated expression of pro-apoptotic activated caspase-3 and Bax, increased expression of anti-apoptotic Bcl-2, and mitigation of Aβ-induced morphological alterations. Regarding its effects on inflammatory responses, PT-3 pre-treatment decreased the expression of pro-inflammatory cytokines IL-1β and IL-6. The mechanisms of PT-3 neuronal protection against inflammation may be associated with the mitogen-activated protein kinases (MAPK) pathway. Aβ1-42-induced phosphorylation of JNK and p38 MAPK was inhibited by pretreatment with PT-3 in a dose-dependent manner. However, phosphorylation of ERK1/2 was not affected by either PT-3 or Aβ1-42. PT-3 did not stimulate Akt phosphorylation, which was inhibited by Aβ1-42. These findings suggest that PT-3 protects neurons from Aβ1-42-induced neurotoxicity through its anti-apoptotic, anti-oxidative, and anti-inflammatory properties with inhibition of JNK and p38 MAPK phosphorylation as the potential underlying mechanism.

Original languageEnglish (US)
Pages (from-to)20-25
Number of pages6
JournalNeuroscience Letters
Volume556
DOIs
StatePublished - Nov 27 2013
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Amyloid β-peptide
  • Anti-inflammation
  • Antioxidant
  • Apoptosis
  • Mechanism
  • N-benzylcinnamide

ASJC Scopus subject areas

  • Neuroscience(all)

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  • Cite this

    Thangnipon, W., Puangmalai, N., Chinchalongporn, V., Jantrachotechatchawan, C., Kitiyanant, N., Soi-ampornkul, R., Tuchinda, P., & Nobsathian, S. (2013). N-benzylcinnamide protects rat cultured cortical neurons from β-amyloid peptide-induced neurotoxicity. Neuroscience Letters, 556, 20-25. https://doi.org/10.1016/j.neulet.2013.09.071