ArticleIn vitro cellular & developmental biology. Animal2021
Therapeutic potential of ginsenoside Rg3 and Rf for Huntington's disease.
Article in In vitro cellular & developmental biology. Animal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Natural products and neurocognitive disorders: Mechanistic insights and research advances (Review).Molecular medicine reports · 2026Review
- A recent review on ginseng's effects on neurodegenerative diseases: active ingredients, mechanisms of action, applications, and delivery strategies.Frontiers in nutrition · 2026Review
- Microbial-Modified Organosilica-Based Dual-Mode Fluorescent Probe for Zn²⁺ and pH Sensing with Potential Application in Gut Immunity Modulation.Journal of fluorescence · 2026Article
- Efficacy and mechanism of action of ginsenoside Rg3 on radiation proctitis in rats.Immunity, inflammation and disease · 2024Article
- Exploring the Potential Therapeutic Approach Using Ginsenosides for the Management of Neurodegenerative Disorders.Molecular biotechnology · 2024Review
- Study insights in the role of PGC-1α in neurological diseases: mechanisms and therapeutic potential.Frontiers in aging neuroscience · 2024Review
- Effects of Red ginseng on neuroinflammation in neurodegenerative diseases.Journal of ginseng research · 2024Review
- Ginsenoside compound K reduces the progression of Huntington's disease via the inhibition of oxidative stress and overactivation of the ATM/AMPK pathway.Journal of ginseng research · 2022Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginseng is a popular herbal medicine and known to have protective and therapeutic effects in various diseases. Ginsenosides are active gradients representing the diverse pharmacological efficacy of ginseng. Huntington's disease (HD) is incurable genetic disorder associated with mutant huntingtin (mHtt) aggregation in the central nervous system. This study was conducted to investigate the effects of ginsenoside Rg3 and Rf on mHtt aggregation, cell viability, mitochondrial function, and apoptotic molecules on HD model. To investigate the effect of ginsenosides on HD, neural stem cells were isolated from the R6/2 mouse brain and used as a cellular model of HD. Nuclear aggregation of mHtt was measured by immunocytochemistry, and expressions of mitochondrial biogenesis and apoptotic molecules were investigated by western blot. As a result, the number of mHtt aggregates positive cells has decreased by ginsenoside Rg3 and Rf treatment in cellular model of HD. Mitochondrial biogenesis-related molecules such as PGC-1α and phosphorylated CREB were increased or showed increased tendency by ginsenoside Rg3 and Rf. Apoptotic molecules, p53, Bax, and cleaved caspase-3, were down-regulated by treatment of ginsenoside Rg3 and Rf. In addition, Lysotracker staining result showed that cellular lysosomal content was reduced by ginsenoside Rg3 and Rf. Given that ginsenoside Rg3 and Rf have the potential to reduce mHtt aggregation and cellular apoptosis, these ginsenosides can be possible therapeutic candidates for treating HD phenotypes.
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