Anti-amnesic effect of ESP-102 on Aβ(1-42)-induced memory impairment in mice

Dong Hyun Kim, Won Young Jung, Se Jin Park, Jong Min Kim, Seungjoo Lee, Young Choong Kim, Jong Hoon Ryu
Pharmacology, Biochemistry, and Behavior 2010, 97 (2): 239-48
The aim of this study was to characterize the effects of ESP-102 on the memory impairments and pathological changes induced by amyloid-β (Aβ)(1-42) peptide in mice. The ameliorating effect of ESP-102 on memory impairment was investigated using the passive avoidance and the Morris water maze tasks, and the pathological changes were identified by immunohistochemistry and western blotting. Aβ(1-42) peptide (3μg/3μl) was administered by intracerebroventricular injection. By the single administration of ESP-102 (100mg/kg, p.o), the memory impairment induced by Aβ(1-42) peptide was significantly attenuated (P<0.05). Moreover, ESP-102 (100mg/kg, p.o) significantly inhibited acetylcholinesterase (AChE) activity in the hippocampus compared to the Aβ(1-42) peptide-injected control group. In the subchronic treatment study, ESP-102 (50 or 100mg/kg/day, p.o) administration for seven days ameliorated the memory impairments induced by Aβ(1-42) peptide. Moreover, ESP-102 inhibited lipid peroxidation induced by Aβ(1-42) peptide in the hippocampus. Aβ(1-42)-induced increases in the expression of GFAP (an astrocyte marker) and inducible nitric oxide synthase (iNOS) in the hippocampal region were also attenuated by ESP-102 treatment. These results suggest that the ameliorating effect of ESP-102 on Aβ(1-42) peptide-induced memory impairment is mediated via its AChE inhibitory, antioxidative, and/or anti-inflammatory activities.

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