Biomol Ther.  2015 Mar;23(2):156-164. 10.4062/biomolther.2014.110.

Spinosin, a C-Glucosylflavone, from Zizyphus jujuba var. spinosa Ameliorates Abeta1-42 Oligomer-Induced Memory Impairment in Mice

Affiliations
  • 1Department of Life and Nanopharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul 130-701, Republic of Korea. jhryu63@khu.ac.kr
  • 2Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University, Seoul 130-701, Republic of Korea.
  • 3Pharmaceutical science, College of Pharmacy, Kyung Hee University, Seoul 130-701, Republic of Korea.
  • 4Kyung Hee East-West Pharmaceutical Research Institute, College of Pharmacy, Kyung Hee University, Seoul 130-701, Republic of Korea.

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder associated with progressive memory loss and neuronal cell death. Although numerous previous studies have been focused on disease progression or reverse pathological symptoms, therapeutic strategies for AD are limited. Alternatively, the identification of traditional herbal medicines or their active compounds has received much attention. The aims of the present study were to characterize the ameliorating effects of spinosin, a C-glucosylflavone isolated from Zizyphus jujuba var. spinosa, on memory impairment or the pathological changes induced through amyloid-beta1-42 oligomer (AbetaO) in mice. Memory impairment was induced by intracerebroventricular injection of AbetaO (50 muM) and spinosin (5, 10, and 20 mg/kg) was administered for 7 days. In the behavioral tasks, the subchronic administration of spinosin (20 mg/kg, p.o.) significantly ameliorated AbetaO-induced cognitive impairment in the passive avoidance task or the Y-maze task. To identify the effects of spinosin on the pathological changes induced through AbetaO, immunohistochemistry and Western blot analyses were performed. Spinosin treatment also reduced the number of activated microglia and astrocytes observed after AbetaO injection. In addition, spinosin rescued the AbetaO-induced decrease in choline acetyltransferase expression levels. These results suggest that spinosin ameliorated memory impairment induced through AbetaO, and these effects were regulated, in part, through neuroprotective activity via the anti-inflammatory effects of spinosin. Therefore, spinosin might be a useful agent against the amyloid b protein-induced cognitive dysfunction observed in AD patients.

Keyword

Spinosin; Amyloid-beta oligomer; Alzheimer's disease; Neuroprotection

MeSH Terms

Alzheimer Disease
Amyloid
Animals
Astrocytes
Blotting, Western
Cell Death
Choline O-Acetyltransferase
Disease Progression
Humans
Immunohistochemistry
Memory Disorders
Memory*
Mice*
Microglia
Neurodegenerative Diseases
Neurons
Ziziphus*
Amyloid
Choline O-Acetyltransferase
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