Xanthoceraside attenuates amyloid β peptide25-35-induced learning and memory impairments in mice

Ping Lu, Takayoshi Mamiya, Lingling Lu, Akihiro Mouri, Takashi Ikejima, Hyoung Chum Kim, Li Bo Zou, Toshitaka Nabeshima

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Rationale: 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. Objectives: The purpose of this study was to examine the effect of xanthoceraside on behavioral impairments, inflammatory responses, and oxidative stress induced by Aβ peptide25-35 (Aβ 25-35) in mice. Materials and methods: The mice were treated orally with xanthoceraside (0.02, 0.08, or 0.32 mg/kg, once daily) after the intracerebroventricular injection of Aβ25-35 (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 Aβ25-35 injection by real-time reverse transcription-polymerase chain reaction. Results: Xanthoceraside significantly attenuated behavioral impairments induced by Aβ25-35 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 Aβ25-35, 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 Aβ25-35 and is a potential candidate for an AD treatment.

Original languageEnglish
Pages (from-to)181-190
Number of pages10
JournalPsychopharmacology
Volume219
Issue number1
DOIs
Publication statusPublished - 01-01-2012
Externally publishedYes

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Amyloid
Learning
Nitric Oxide Synthase Type II
Hippocampus
Oxidative Stress
Interleukin-4
Alzheimer Disease
Messenger RNA
Injections
xanthoceraside
Cognition
Reverse Transcription
Anti-Inflammatory Agents
Polymerase Chain Reaction
Peptides
Therapeutics

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Lu, Ping ; Mamiya, Takayoshi ; Lu, Lingling ; Mouri, Akihiro ; Ikejima, Takashi ; Kim, Hyoung Chum ; Zou, Li Bo ; Nabeshima, Toshitaka. / Xanthoceraside attenuates amyloid β peptide25-35-induced learning and memory impairments in mice. In: Psychopharmacology. 2012 ; Vol. 219, No. 1. pp. 181-190.
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abstract = "Rationale: 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. Objectives: The purpose of this study was to examine the effect of xanthoceraside on behavioral impairments, inflammatory responses, and oxidative stress induced by Aβ peptide25-35 (Aβ 25-35) in mice. Materials and methods: The mice were treated orally with xanthoceraside (0.02, 0.08, or 0.32 mg/kg, once daily) after the intracerebroventricular injection of Aβ25-35 (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 Aβ25-35 injection by real-time reverse transcription-polymerase chain reaction. Results: Xanthoceraside significantly attenuated behavioral impairments induced by Aβ25-35 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 Aβ25-35, 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 Aβ25-35 and is a potential candidate for an AD treatment.",
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Xanthoceraside attenuates amyloid β peptide25-35-induced learning and memory impairments in mice. / Lu, Ping; Mamiya, Takayoshi; Lu, Lingling; Mouri, Akihiro; Ikejima, Takashi; Kim, Hyoung Chum; Zou, Li Bo; Nabeshima, Toshitaka.

In: Psychopharmacology, Vol. 219, No. 1, 01.01.2012, p. 181-190.

Research output: Contribution to journalArticle

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AB - Rationale: 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. Objectives: The purpose of this study was to examine the effect of xanthoceraside on behavioral impairments, inflammatory responses, and oxidative stress induced by Aβ peptide25-35 (Aβ 25-35) in mice. Materials and methods: The mice were treated orally with xanthoceraside (0.02, 0.08, or 0.32 mg/kg, once daily) after the intracerebroventricular injection of Aβ25-35 (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 Aβ25-35 injection by real-time reverse transcription-polymerase chain reaction. Results: Xanthoceraside significantly attenuated behavioral impairments induced by Aβ25-35 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 Aβ25-35, 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 Aβ25-35 and is a potential candidate for an AD treatment.

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