Ginsenoside Rg1 Attenuates Oligomeric Aβ1-42-Induced Mitochondrial Dysfunction

Title:Ginsenoside Rg1 Attenuates Oligomeric Aβ1-42-Induced Mitochondrial Dysfunction

Volume: 9 Issue: 3

Author(s): Tianwen Huang, Fang Fang, Limin Chen, Yuangui Zhu, Jing Zhang, Xiaochun Chen and Shirley Shidu Yan

Affiliation:

Keywords: Alzheimer’s disease, oligomeric beta-amyloid peptide1-42, mitochondria, ginsenoside Rg1

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.

Cite this article as:

Huang Tianwen, Fang Fang, Chen Limin, Zhu Yuangui, Zhang Jing, Chen Xiaochun and Shidu Yan Shirley, Ginsenoside Rg1 Attenuates Oligomeric Aβ1-42-Induced Mitochondrial Dysfunction, Current Alzheimer Research 2012; 9 (3) . https://dx.doi.org/10.2174/156720512800107636