Nutr Res Pract.  2014 Aug;8(4):386-390.

Protective effects of Acanthopanax divaricatus extract in mouse models of Alzheimer's disease

Affiliations
  • 1Department of Pharmacology, College of Medicine, Hallym University, 1 Hallymdaehak-gil, Chuncheon, Gangwon 200-702, Korea. dksong@hallym.ac.kr

Abstract

BACKGROUND
Acanthopanax divaricatus var. albeofructus (ADA) extract has been reported to have anti-oxidant, immunomodulatory, and anti-mutagenic activity.
MATERIALS/METHODS
We investigated the effects of ADA extract on two mouse models of Alzheimer's disease (AD); intracerebroventricular injection of beta-amyloid peptide (Abeta) and amyloid precursor protein/presenilin 1 (APP/PS1)-transgenic mice.
RESULTS
Intra-gastric administration of ADA stem extract (0.25 g/kg, every 12 hrs started from one day prior to injection of Abeta1-42 until evaluation) effectively blocked Abeta1-42-induced impairment in passive avoidance performance, and Abeta1-42-induced increase in immunoreactivities of glial fibrillary acidic protein and interleukin (IL)-1alpha in the hippocampus. In addition, it alleviated the Abeta1-42-induced decrease in acetylcholine and increase in malondialdehyde levels in the cortex. In APP/PS1-transgenic mice, chronic oral administration of ADA stem extract (0.1 or 0.5 g/kg/day for six months from the age of six to 12 months) resulted in significantly enhanced performance of the novel-object recognition task, and reduced amyloid deposition and IL-1beta in the brain.
CONCLUSIONS
The results of this study suggest that ADA stem extract may be useful for prevention and treatment of AD.

Keyword

Alzheimer disease; Acanthopanax divaricatus; beta-amyloid peptide; amyloid precursor protein/presenilin 1

MeSH Terms

Eleutherococcus*
Acetylcholine
Administration, Oral
Alzheimer Disease*
Amyloid
Animals
Brain
Glial Fibrillary Acidic Protein
Hippocampus
Interleukins
Malondialdehyde
Mice*
Plaque, Amyloid
Acetylcholine
Amyloid
Glial Fibrillary Acidic Protein
Interleukins
Malondialdehyde

Figure

  • Fig. 1 Experimental schedules for evaluation of the effects of ADA extract on mouse models of i.c.v. injection of Aβ1-42 (A) and APP/PS1-transgenic mice (B).

  • Fig. 2 Protective effect of ADA stem extract on Aβ1-42-induced impairment of passive avoidance performance. (A). ADA stem extract (0.25 g/kg or 0.5 g/kg) was administered intra-gastrically every 12 hrs, five times (two times prior to Aβ1-42 treatment, and three times post-Aβ1-42 treatment). Passive avoidance test was performed one day after Aβ1-42 treatment. (B). Effects of different parts of ADA extract (0.25 g/kg) given with the same protocol on the Aβ1-42-induced impairment of passive avoidance performance. *P < 0.05, **P < 0.01 vs control. #P < 0.05, ##P < 0.01 vs Aβ1-42 alone. Data are expressed as mean ± SEM (n = 10-12).

  • Fig. 3 Protective effects of ADA stem extract on Aβ1-42-induced changes in cortical acetylcholine (ACh) and malondialdehyde (MDA) as well as hippocampal GFAP- and IL-1α-immunoreactivities. ADA stem extract (0.25 g/kg) was administered intra-gastrically every 12 hrs for six days (from one day before Aβ1-42 treatment to five days post-Aβ1-42 treatment), and evaluation was performed five days after Aβ1-42 treatment. *P < 0.05, **P < 0.01 vs control. #P < 0.05 vs Aβ 1-42 alone. Data are expressed as mean ± SEM (n = 10).

  • Fig. 4 Effect of ADA stem extract treatment for six months on body weight (A), novel-object recognition task (B), brain Aβ (C,D) and IL-1β (E) levels in APP/PS1-transgenic mice at 12 months of age. *P < 0.05, **P < 0.01, ***P < 0.001 vs control. #P < 0.05 vs ADA (0.1 g/kg/day). Data are expressed as mean ± SEM (a: 0 and two months, n = 4, 5, 5 for control, 0.1 g/kg/day, 0.5 g/kg/day, respectively; six months, n = 3, 5, 4 for control, 0.1 g/kg/day, 0.5 g/kg/day, respectively; b-e: n = 3, 5, 4 for control, 0.1 g/kg/day, 0.5 g/kg/day, respectively).


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