ArticleJournal of ginseng research2023
Ginsenoside F2 enhances glucose metabolism by modulating insulin signal transduction in human hepatocarcinoma cells.
Article in Journal of ginseng research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Emerging and underexplored ginsenosides in cancer therapy (2020-2025): Beyond cytotoxic mechanisms.Journal of ginseng research · 2026Review
- Mechanistic insights into the regulation of glucose‒lipid metabolism by the bioactive constituents of ginseng.Journal of ginseng research · 2026Review
- Protopanaxatriol, a ginsenoside metabolite, induces apoptosis in colorectal cancer cells and arrests their cell cycle by targeting AKT.Journal of ginseng research · 2025Article
- The Effects of Engeletin on Insulin Resistance Induced in Human HepG2 Liver Cells.Current issues in molecular biology · 2025Article
- Article
- Ameliorative Effects of Curcumin on Type 2 Diabetes Mellitus.Molecules (Basel, Switzerland) · 2024Review
- Attenuation of senile pruritus by PAC-14028-mediated downregulation of the NF-κB and MAPK pathways.International journal of immunopathology and pharmacologyArticle
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Ginsenoside F2 (GF2), a minor component of Methods: HepG2 cells were used to establish insulin-resistant (IR) model and treated with GF2. Cell viability and glucose uptake-related genes were also examined by real-time PCR and immunoblots. Results: Cell viability assays showed that GF2 up to 50 μM did not affect normal and IR-HepG2 cell viability. GF2 reduced oxidative stress by inhibiting phosphorylation of the mitogen-activated protein kinases (MAPK) signaling components such as c-Jun N-terminal kinase (JNK), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 MAPK, and reducing the nuclear translocation of NF-κB. Furthermore, GF2 activated PI3K/AKT signaling, upregulated the levels of glucose transporter 2 (GLUT-2) and GLUT-4 in IR-HepG2 cells, and promoted glucose absorption. At the same time, GF2 reduced phosphoenolpyruvate carboxykinase and glucose-6-phosphatase expression as well as inhibiting gluconeogenesis. Conclusion: Overall, GF2 improved glucose metabolism disorders by reducing cellular oxidative stress in IR-HepG2 cells via MAPK signaling, participating in the PI3K/AKT/GSK-3β signaling pathway, promoting glycogen synthesis, and inhibiting gluconeogenesis.
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