Abstract
Oxidative stress and mitochondrial dysfunction appear early and contribute to the disease progression in Alzheimer’s disease (AD), which can be detected extensively in AD patients brains as well as in transgenic AD mice brains. Thus, treatments that result in attenuation of oxidative stress and mitochondrial dysfunction may hold potential for AD treatment. Geniposide, a pharmacologically active component purified from gardenia fruit, exhibits anti-oxidative, antiinflammatory and other important therapeutic properties. However, whether geniposide has any protective effect on oxidative stress and mitochondrial dysfunction in AD transgenic mouse model has not yet been reported. Here, we demonstrate that intragastric administration of geniposide significantly reduces oxidative stress and mitochondrial dysfunction in addition to improving learning and memory in APP/PS1 mice. Geniposide exerts protective effects on mitochondrial dysfunction in APP/PS1 mice through suppressing the mitochondrial oxidative damage and increasing the mitochondrial membrane potential and activity of cytochrome c oxidase. These studies indicate that geniposide may attenuate memory deficits through the suppression of mitochondrial oxidative stress. Thus, geniposide may be a potential therapeutic reagent for halting and preventing AD progress.
Keywords: Alzheimer’s disease, APP/PS1 transgenic mice, cytochrome c oxidase, geniposide, mitochondrial dysfunction, oxidative stress.
Current Alzheimer Research
Title:Geniposide Attenuates Mitochondrial Dysfunction and Memory Deficits in APP/PS1 Transgenic Mice
Volume: 11 Issue: 6
Author(s): Cui Lv, Xiaoli Liu, Hongjuan Liu, Tong Chen and Wensheng Zhang
Affiliation:
Keywords: Alzheimer’s disease, APP/PS1 transgenic mice, cytochrome c oxidase, geniposide, mitochondrial dysfunction, oxidative stress.
Abstract: Oxidative stress and mitochondrial dysfunction appear early and contribute to the disease progression in Alzheimer’s disease (AD), which can be detected extensively in AD patients brains as well as in transgenic AD mice brains. Thus, treatments that result in attenuation of oxidative stress and mitochondrial dysfunction may hold potential for AD treatment. Geniposide, a pharmacologically active component purified from gardenia fruit, exhibits anti-oxidative, antiinflammatory and other important therapeutic properties. However, whether geniposide has any protective effect on oxidative stress and mitochondrial dysfunction in AD transgenic mouse model has not yet been reported. Here, we demonstrate that intragastric administration of geniposide significantly reduces oxidative stress and mitochondrial dysfunction in addition to improving learning and memory in APP/PS1 mice. Geniposide exerts protective effects on mitochondrial dysfunction in APP/PS1 mice through suppressing the mitochondrial oxidative damage and increasing the mitochondrial membrane potential and activity of cytochrome c oxidase. These studies indicate that geniposide may attenuate memory deficits through the suppression of mitochondrial oxidative stress. Thus, geniposide may be a potential therapeutic reagent for halting and preventing AD progress.
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Cite this article as:
Lv Cui, Liu Xiaoli, Liu Hongjuan, Chen Tong and Zhang Wensheng, Geniposide Attenuates Mitochondrial Dysfunction and Memory Deficits in APP/PS1 Transgenic Mice, Current Alzheimer Research 2014; 11 (6) . https://dx.doi.org/10.2174/1567205011666140618095925
DOI https://dx.doi.org/10.2174/1567205011666140618095925 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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