ArticleJournal of ginseng research2020
Gintonin stimulates autophagic flux in primary cortical astrocytes.
Article in Journal of ginseng research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
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- Antae-eum, a herbal formula, relieves LPS-induced inflammatory response in macrophages via suppression of autophagic flux.Scientific reports · 2025Article
- Advancements in Autophagy Modulation for the Management of Oral Disease: A Focus on Drug Targets and Therapeutics.Biomedicines · 2024Review
- Autophagy and Female Fertility: Mechanisms, Clinical Implications, and Emerging Therapies.Cells · 2024Review
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- Autophagy Modulation in Aggresome Formation: Emerging Implications and Treatments of Alzheimer's Disease.Biomedicines · 2022Review
- Progress on the Elucidation of the Antinociceptive Effect of Ginseng and Ginsenosides in Chronic Pain.Frontiers in pharmacology · 2022Review
- Antioxidant and Anti-Inflammatory Effects of 3-Dehydroxyceanothetric Acid 2-Methyl Ester Isolated fromBiomolecules · 2021Article
- TNF-α-induced protein 8-like 2 negatively regulates the immune function of dendritic cells by suppressing autophagy via the TAK1/JNK pathway in septic mice.Cell death & disease · 2021Article
- 4,6'-Anhydrooxysporidinone fromBiomolecules · 2021Article
- Antioxidant Compound, Oxyresveratrol, Inhibits APP Production through the AMPK/ULK1/mTOR-Mediated Autophagy Pathway in Mouse Cortical Astrocytes.Antioxidants (Basel, Switzerland) · 2021Article
- Ginseng gintonin, aging societies, and geriatric brain diseases.Integrative medicine research · 2021Review
- Phytochemicals as a Complement to Cancer Chemotherapy: Pharmacological Modulation of the Autophagy-Apoptosis Pathway.Frontiers in pharmacology · 2021Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundGintonin (GT), a novel ginseng-derived exogenous ligand of lysophosphatidic acid (LPA) receptors, has been shown to induce cell proliferation and migration in the hippocampus, regulate calcium-dependent ion channels in the astrocytes, and reduce β-amyloid plaque in the brain. However, whether GT influences autophagy in cortical astrocytes is not yet investigated.
methodsWe examined the effect of GT on autophagy in primary cortical astrocytes using immunoblot and immunocytochemistry assays. Suppression of specific proteins was performed via siRNA. LC3 puncta was determined using confocal microscopy.
resultsGT strongly upregulated autophagy marker LC3 by a concentration- as well as time-dependent manner via G protein-coupled LPA receptors. GT-induced autophagy was further confirmed by the formation of LC3 puncta. Interestingly, on pretreatment with an mammalian target of rapamycin (mTOR) inhibitor, rapamycin, GT further enhanced LC3-II and LC3 puncta expression. However, GT-induced autophagy was significantly attenuated by inhibition of autophagy by 3-methyladenine and knockdown Beclin-1, Atg5, and Atg7 gene expression. Importantly, when pretreated with a lysosomotropic agent, E-64d/peps A or bafilomycin A1, GT significantly increased the levels of LC3-II along with the formation of LC3 puncta. In addition, GT treatment enhanced autophagic flux, which led to an increase in lysosome-associated membrane protein 1 and degradation of ubiquitinated p62/SQSTM1.
conclusionGT induces autophagy via mTOR-mediated pathway and elevates autophagic flux. This study demonstrates that GT can be used as an autophagy-inducing agent in cortical astrocytes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.