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Xanthoceraside attenuates amyloid β peptide₂₅₋₃₅-induced learning and memory impairments in mice.
Psychopharmacology (Berl). 2012 Jan; 219(1):181-90.P

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 peptide(25-35) (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 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+Show Affiliations

Department of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, Meijo University, 150 Yagotoyama, Tempaku-ku, Nagoya 468-8503, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

21735075

Citation

Lu, Ping, et al. "Xanthoceraside Attenuates Amyloid Β Peptide₂₅₋₃₅-induced Learning and Memory Impairments in Mice." Psychopharmacology, vol. 219, no. 1, 2012, pp. 181-90.
Lu P, Mamiya T, Lu L, et al. Xanthoceraside attenuates amyloid β peptide₂₅₋₃₅-induced learning and memory impairments in mice. Psychopharmacology (Berl). 2012;219(1):181-90.
Lu, P., Mamiya, T., Lu, L., Mouri, A., Ikejima, T., Kim, H. C., Zou, L. B., & Nabeshima, T. (2012). Xanthoceraside attenuates amyloid β peptide₂₅₋₃₅-induced learning and memory impairments in mice. Psychopharmacology, 219(1), 181-90. https://doi.org/10.1007/s00213-011-2386-1
Lu P, et al. Xanthoceraside Attenuates Amyloid Β Peptide₂₅₋₃₅-induced Learning and Memory Impairments in Mice. Psychopharmacology (Berl). 2012;219(1):181-90. PubMed PMID: 21735075.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Xanthoceraside attenuates amyloid β peptide₂₅₋₃₅-induced learning and memory impairments in mice. AU - Lu,Ping, AU - Mamiya,Takayoshi, AU - Lu,Lingling, AU - Mouri,Akihiro, AU - Ikejima,Takashi, AU - Kim,Hyoung-Chum, AU - Zou,Li-Bo, AU - Nabeshima,Toshitaka, Y1 - 2011/07/07/ PY - 2011/02/10/received PY - 2011/06/13/accepted PY - 2011/7/8/entrez PY - 2011/7/8/pubmed PY - 2012/9/21/medline SP - 181 EP - 90 JF - Psychopharmacology JO - Psychopharmacology (Berl.) VL - 219 IS - 1 N2 - 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 peptide(25-35) (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 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. SN - 1432-2072 UR - https://www.unboundmedicine.com/medline/citation/21735075/Xanthoceraside_attenuates_amyloid_β_peptide₂₅₋₃₅_induced_learning_and_memory_impairments_in_mice_ L2 - https://dx.doi.org/10.1007/s00213-011-2386-1 DB - PRIME DP - Unbound Medicine ER -