Affordable Access

Access to the full text

Phytoceramide ameliorates ß-amyloid protein-induced memory impairment and neuronal death in mice

Authors
  • Jang, Ji Yeon1
  • Lee, Hong Kyu1
  • Yoo, Hwan-Su2
  • Seong, Yeon Hee1
  • 1 Chungbuk National University, College of Veterinary Medicine and Veterinary Medical Center, Cheongju, 28644, Republic of Korea , Cheongju (South Korea)
  • 2 Chungbuk National University, College of Pharmacy, Cheongju, 28160, Republic of Korea , Cheongju (South Korea)
Type
Published Article
Journal
Archives of Pharmacal Research
Publisher
Springer-Verlag
Publication Date
Jun 09, 2017
Volume
40
Issue
6
Pages
760–771
Identifiers
DOI: 10.1007/s12272-017-0893-2
Source
Springer Nature
Keywords
License
Yellow

Abstract

The present study was performed to investigate the protective effect of phytoceramide against ß-amyloid protein (Aβ) (25–35)-induced memory impairment and its underlying mechanisms in mice. Memory impairment in mice was induced by intracerebroventricular injection of 15 nmol Aβ (25–35) and measured by the passive avoidance test and Morris water maze test. Chronic administration of phytoceramide (10, 25 and 50 mg/kg, p.o.) resulted in significantly less Aβ (25–35)-induced memory loss and hippocampal neuronal death in treated mice compared to controls. The decrease of glutathione level and increase of lipid peroxidation in brain tissue following injection of Aβ (25–35) was reduced by phytoceramide. Alteration of apoptosis-related proteins, increase of inflammatory factors, and phosphorylation of mitogen activated proteins kinases (MAPKs) in Aβ (25–35)-administered mice hippocampus were inhibited by phytoceramide. Phosphatidylinositol 3′-kinase (PI3K)/Akt pathway and phosphorylation of cyclic AMP response element-binding protein (CREB) were suppressed, while phosphorylation of tau (p-tau) was increased in Aß (25–35)-treated mice brain; these effects were significantly inhibited by administration of phytoceramide. These results suggest that phytoceramide has a possible therapeutic role in managing cognitive impairment associated with Alzheimer’s disease. The underlying mechanism might involve inhibition of p-tau formation via anti-apoptosis and anti-inflammation activity and promotion of PI3K/Akt/CREB signaling process.

Report this publication

Statistics

Seen <100 times