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 language | English |
|---|---|
| Pages (from-to) | 181-190 |
| Number of pages | 10 |
| Journal | Psychopharmacology |
| Volume | 219 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 01-01-2012 |
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All Science Journal Classification (ASJC) codes
- Pharmacology
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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 journal › Article
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
PY - 2012/1/1
Y1 - 2012/1/1
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 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.
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.
UR - http://www.scopus.com/inward/record.url?scp=84856643383&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84856643383&partnerID=8YFLogxK
U2 - 10.1007/s00213-011-2386-1
DO - 10.1007/s00213-011-2386-1
M3 - Article
C2 - 21735075
AN - SCOPUS:84856643383
VL - 219
SP - 181
EP - 190
JO - Psychopharmacology
JF - Psychopharmacology
SN - 0033-3158
IS - 1
ER -