title: Xanthoceraside attenuates amyloid β peptide₂₅₋₃₅-induced learning and memory impairments in mice.
abstract: BACKGROUND
  In Alzheimer's disease (AD), the deposition of amyloid peptides is invariably associated with oxidative stress and inflammatory responses. Xanthoceraside has anti-inflammatory and antioxidative activities. However, it remains unclear whether xanthoceraside improves amyloid β (Aβ)-induced neurotoxicity.
  
  
  OBJECTIVE
  The purpose of this study was to examine the effect of xanthoceraside on behavioral impairments, inflammatory responses, and oxidative stress induced by Aβ peptide(25-35) (Aβ(25-35)) in mice.
  
  
  METHODS
  The mice were treated orally with xanthoceraside (0.02, 0.08, or 0.32 mg/kg, once daily) after the intracerebroventricular injection of Aβ(25-35) (day 0). Cognitive functions were evaluated in Y-maze (day 6) and novel object recognition tests (days 7 and 8). Inducible nitric oxide synthase (iNOS) and nitrotyrosine levels in the hippocampus were examined (day 9). The mRNA expressions of iNOS and interleukin-4 (IL-4) in the hippocampus were measured 2 h and 3 days after the Aβ(25-35) injection by real-time reverse transcription-polymerase chain reaction.
  
  
  RESULTS
  Xanthoceraside significantly attenuated behavioral impairments induced by Aβ(25-35) in the Y-maze and novel object recognition tests. Repeated treatment with xanthoceraside significantly inhibited the increase in the expression of iNOS and nitrotyrosine in the hippocampus induced by Aβ(25-35), which is associated with an enhanced expression of the IL-4 mRNA.
  
  
  CONCLUSIONS
  These findings suggest that xanthoceraside attenuates memory impairments through amelioration of oxidative stress and inflammatory responses induced by Aβ(25-35) and is a potential candidate for an AD treatment.
authors: Department of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Meijo University, 150 Yagotoyama, Tempaku-ku, Nagoya 468-8503, Japan.
authors: Ping
authors: P
authors: Lu
authors: Takayoshi
authors: T
authors: Mamiya
authors: Lingling
authors: L
authors: Lu
authors: Akihiro
authors: A
authors: Mouri
authors: Takashi
authors: T
authors: Ikejima
authors: Hyoung-Chum
authors: HC
authors: Kim
authors: Li-Bo
authors: LB
authors: Zou
authors: Toshitaka
authors: T
authors: Nabeshima
mesh_terms: D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D008297:Male; D018782:Maze Learning / Q000187:drug effects* / Q000502:physiology; D008569:Memory Disorders / Q000139:chemically induced / Q000378:metabolism / Q000517:prevention & control*; D051379:Mice; D008813:Mice, Inbred ICR; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D010446:Peptide Fragments / Q000633:toxicity*; D012503:Saponins / Q000494:pharmacology / Q000627:therapeutic use*; D014315:Triterpenes / Q000494:pharmacology / Q000627:therapeutic use*
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; D012503:Saponins; D014315:Triterpenes; C074636:amyloid beta-protein (25-35); C548611:xanthoceraside