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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Alzheimer Disease / drug therapy*
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Alzheimer Disease / metabolism
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Alzheimer Disease / pathology
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Amyloid beta-Peptides / antagonists & inhibitors*
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Amyloid beta-Peptides / toxicity
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Animals
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Cell Death / drug effects
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Cell Death / physiology
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Cell Survival / drug effects
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Cell Survival / physiology
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Central Nervous System Agents / chemistry
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Central Nervous System Agents / pharmacology
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Female
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Ginsenosides / chemistry
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Ginsenosides / pharmacology*
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Mice
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Mice, Inbred C57BL
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Mitochondrial Diseases / drug therapy*
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Mitochondrial Diseases / metabolism
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Mitochondrial Diseases / pathology
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Nerve Degeneration / drug therapy*
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Nerve Degeneration / metabolism
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Nerve Degeneration / pathology
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Neuroprotective Agents / chemistry
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Neuroprotective Agents / pharmacology*
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Peptide Fragments / antagonists & inhibitors*
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Peptide Fragments / toxicity
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Primary Cell Culture
Substances
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Amyloid beta-Peptides
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Central Nervous System Agents
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Ginsenosides
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Neuroprotective Agents
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Peptide Fragments
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amyloid beta-protein (1-42)
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ginsenoside Rg1