ArticleRedox biology2020
Ginsenoside Rh2 pretreatment and withdrawal reactivated the pentose phosphate pathway to ameliorate intracellular redox disturbance and promoted intratumoral penetration of adriamycin.
Article in Redox biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Ginsenosides Rh2 and Rg3 in first-line combination therapy: Prospects for rapid clinical translation in drug-resistant triple-negative breast cancer.Journal of ginseng research · 2026Review
- Synergistic mechanical and therapeutic modulation of engineered tumor cell-derived microparticles for enhanced cancer treatment.Cell reports. Medicine · 2026Article
- Ginsenoside Rh2 shifts tumor metabolism from aerobic glycolysis to oxidative phosphorylation through regulating the HIF1-α/PDK4 axis in non-small cell lung cancer.Molecular medicine (Cambridge, Mass.) · 2024Article
- LncRNA MAFG-AS1 is involved in human cancer progression.European journal of medical research · 2023Review
- The ways for ginsenoside Rh2 to fight against cancer: the molecular evidencesJournal of ginseng research · 2023Review
- Adriamycin induces cardiac fibrosis in mice via PRMT5-mediated cardiac fibroblast activation.Acta pharmacologica Sinica · 2023Article
- Tumor cell membrane-camouflaged responsive nanoparticles enable MRI-guided immuno-chemodynamic therapy of orthotopic osteosarcoma.Bioactive materials · 2022Article
- Probable Mechanisms of Doxorubicin Antitumor Activity Enhancement by Ginsenoside Rh2.Molecules (Basel, Switzerland) · 2022Article
- Bevacizumab-Induced Mitochondrial Dysfunction, Endoplasmic Reticulum Stress, and ERK Inactivation Contribute to Cardiotoxicity.Oxidative medicine and cellular longevity · 2021Article
- Astragaloside IV Attenuates the Myocardial Injury Caused by Adriamycin by Inhibiting Autophagy.Frontiers in pharmacology · 2021Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Improving the limited penetration, accumulation and therapeutic effects of antitumor drugs in the avascular region of the tumor mass is crucial during chemotherapy. P-gp inhibitors have achieved little success despite significant efforts. Excessive P-gp inhibition disturbed the kinetic balance between intracellular accumulation and intercellular penetration, thus resulting in a more inhomogeneous distribution of substrate drugs. Here, we found that ginsenoside Rh2 pretreatment mildly downregulated P-gp expression through reactivating the pentose phosphate pathway and rebalancing redox status. This mild P-gp inhibition not only significantly increased the growth inhibition effect and accumulation profile of adriamycin (ADR) throughout the multicellular tumor spheroid (MCTS) but also had unique advantages in improving drug penetration. Furthermore, we developed a novel individual-cell-based PK-PD integrated model and proved that metabolic reprogramming and redox rebalancing-based P-gp regulation was sufficient to increase the ADR effect in both central and peripheral cells of MCTS. Thus, a "ginsenoside Rh2-ADR" sequential regimen was proposed and exhibited a potent antitumor effect in vivo. This novel P-gp inhibition via metabolic reprogramming and redox rebalancing provided a new idea for achieving better antitumor effects in the tumor avascular region during chemotherapy.
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