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Ginsenoside Rg1 Attenuates Oligomeric Aβ1-42-Induced Mitochondrial Dysfunction
Huang, Tianwen Fang, Fang Chen, Limin Zhu, Yuangui Zhang, Jing Chen, Xiaochun Yan, Shirley ShiDu
Huang, Tianwen
Fang, Fang
Chen, Limin
Zhu, Yuangui
Zhang, Jing
Chen, Xiaochun
Yan, Shirley ShiDu
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Abstract
Mitochondrial dysfunction is one of the major pathological changes seen in Alzheimer's disease (AD). Amyloid beta-peptide (Aβ), a neurotoxic peptide, accumulates in the brain of AD subjects and mediates mitochondrial and neuronal stress. Therefore, protecting mitochondrion from Aβ-induced toxicity holds potential benefits for halting and treating and perhaps preventing AD. Here, we report that administration of ginsenoside Rg1, a known neuroprotective drug, to primary cultured cortical neurons, rescues Aβ-mediated mitochondrial dysfunction as shown by increases in mitochondrial membrane potential, ATP levels, activity of cytochrome c oxidase (a key enzyme associated with mitochondrial respiratory function), and decreases in cytochrome c release. The protective effects of Rg1 on mitochondrial dysfunction correlate to neuronal injury in the presence of Aβ. This finding suggests that ginsenoside Rg1 may attenuate Aβ-induced neuronal death through the suppression of intracellular mitochondrial oxidative stress and may rescue neurons in AD.
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Date
2013-03-01
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Publisher
Bentham Science Publishers
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Keywords
Alzheimer's disease, Oligmeric beta-amyloid peptide 1-42, Mitochondria, Ginsenoside Rg1
Citation
Huang, Tianwen, Fang Fang, Limin Chen, Yuangui Zhu, Jing Zhang, Xiaochun Chen, and Shirley Shidu Yan. "Ginsenoside Rg1 Attenuates Oligomeric Aβ1-42-Induced Mitochondrial Dysfunction." Current Alzheimer Research 9.3 (2012): 388-95.