a b s t r a c t
Centella asiatica (雷公根lei gong gen) is a traditional medicinal herb with high antioxidant activity, which
decreases amyloid-b (Ab) deposition in the brain. At the same time, aggregated Ab-induced oxidative
stress is the trigger in the pathogenesis of Alzheimer's disease (AD). Here, we investigated the ability of C.
asiatica ethanol extract (CAE) to protect PC12 and IMR32 cells from Ab1e40-induced production of
reactive oxygen species (ROS) and concomitant neurotoxicity. Aggregated Ab1e40 treatment resulted in
reduced cell viability, which can be reversed by cotreatment with 25, 50, and 100 mg/mL CAE. Moreover,
CAE eliminated the Ab1e40-mediated increase in ROS production. Thus, CAE-mediated protection against
aggregated Ab1e40-induced neurotoxicity is attributable to modulation of the antioxidative defense
system in cells, including the activities of superoxide dismutase, catalase, glutathione peroxidase,
glutathione reductase, and levels of glutathione and glutathione disulfide by CAE. This emphasizes the
potential therapeutic and preventive value of CAE in the treatment of AD.
Copyright © 2015, Center for Food and Biomolecules, National Taiwan University. Production and hosting
by Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license
a b s t r a c tCentella asiatica (雷公根lei gong gen) is a traditional medicinal herb with high antioxidant activity, whichdecreases amyloid-b (Ab) deposition in the brain. At the same time, aggregated Ab-induced oxidativestress is the trigger in the pathogenesis of Alzheimer's disease (AD). Here, we investigated the ability of C.asiatica ethanol extract (CAE) to protect PC12 and IMR32 cells from Ab1e40-induced production ofreactive oxygen species (ROS) and concomitant neurotoxicity. Aggregated Ab1e40 treatment resulted inreduced cell viability, which can be reversed by cotreatment with 25, 50, and 100 mg/mL CAE. Moreover,CAE eliminated the Ab1e40-mediated increase in ROS production. Thus, CAE-mediated protection againstaggregated Ab1e40-induced neurotoxicity is attributable to modulation of the antioxidative defensesystem in cells, including the activities of superoxide dismutase, catalase, glutathione peroxidase,glutathione reductase, and levels of glutathione and glutathione disulfide by CAE. This emphasizes thepotential therapeutic and preventive value of CAE in the treatment of AD.Copyright © 2015, Center for Food and Biomolecules, National Taiwan University. Production and hostingby Elsevier Taiwan LLC. This is an open access article under the CC BY-NC-ND license
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