ArticleMolecular medicine reports2017
Ginsenoside Rh2 and Rg3 inhibit cell proliferation and induce apoptosis by increasing mitochondrial reactive oxygen species in human leukemia Jurkat cells.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 52 citations in OpenAlex.
- Research Progress on Anticancer Mechanism of Ginsenoside Regulating Tumor Microenvironment.Current issues in molecular biology · 2026Review
- Ginsenoside Rg1 as a Multifunctional Therapeutic Agent: Pharmacological Properties, Molecular Mechanisms and Clinical Perspectives in Complementary Medicine.Food science & nutrition · 2026Review
- Natural supplements in breast cancer therapy: translational evidence, clinical safety, and emerging challenges.Frontiers in oncology · 2026Review
- Current mechanistic insights into Withaferin A: a promising potential adjuvant anticancer agent from Withania somnifera.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Notoginsenoside R1 Attenuates H/R Injury in H9c2 Cells by Maintaining Mitochondrial Homeostasis.Current issues in molecular biology · 2025Article
- Ginsenoside Rh2 regulates triple-negative breast cancer proliferation and apoptosis via the IL-6/JAK2/STAT3 pathway.Frontiers in pharmacology · 2024Article
- Anti-leukemia effects of ginsenoside monomer: A narrative review of pharmacodynamics study.Current therapeutic research, clinical and experimental · 2024Review
- The ways for ginsenoside Rh2 to fight against cancer: the molecular evidencesJournal of ginseng research · 2023Review
- Microorganisms for Ginsenosides Biosynthesis: Recent Progress, Challenges, and Perspectives.Molecules (Basel, Switzerland) · 2023Review
- Anticancer therapeutic effect of ginsenosides through mediating reactive oxygen species.Frontiers in pharmacology · 2023Review
- Rg3 and Rh2 ginsenosides suppress embryoid body formation by inhibiting the epithelial-mesenchymal transition.Archives of pharmacal research · 2022Article
- Ginsenoside Rh2 inhibits breast cancer cell growth via ERβ-TNFα pathway.Acta biochimica et biophysica Sinica · 2022Article
- Ginsenoside Rb1 selectively improved keratinocyte functions in vitro without affecting tissue regeneration in zebrafish larvae tail regrowth.In vitro cellular & developmental biology. Animal · 2022Article
- The involvement of Parkin-dependent mitophagy in the anti-cancer activity of Ginsenoside.Journal of ginseng research · 2022Article
- Novel molecules as the emerging trends in cancer treatment: an update.Medical oncology (Northwood, London, England) · 2022Review
- Ginseng of different ages is affected by the accumulation of heavy metals in ginseng soil.PloS one · 2022Article
- The promising therapeutic potentials of ginsenosides mediated through p38 MAPK signaling inhibition.Heliyon · 2021Review
- Review of ginsenosides targeting mitochondrial function to treat multiple disorders: Current status and perspectives.Journal of ginseng research · 2021Review
- 20(S)-Ginsenoside Rh2 displays efficacy against T-cell acute lymphoblastic leukemia through the PI3K/Akt/mTOR signal pathway.Journal of ginseng research · 2020Article
- Proteomic analyses reveal that ginsenoside Rg3(Journal of ginseng research · 2020Article
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ginsenoside Rh2 (GRh2) and ginsenoside Rg3 (GRg3) are primary bioactive components in Panax ginseng. The present study aimed to investigate the underlying mechanisms of apoptotic cell‑death induced by GRh2 and GRg3 in human leukemia Jurkat cells. The Cell Counting kit‑8 assay was used to determine cell proliferation. Apoptosis was detected by nuclear morphologic observation by Hoechst 33342 staining and Annexin V-allophycocyanin and 7-amino-actinomycin D assay. mitoTEMPO, a mitochondrial reactive oxygen species (ROS) scavenger, was used to examine the effects of mitochondrial ROS on cell viability and mitochondrial membrane potential (MMP). Finally, the expression levels of numerous mitochondrial‑associated apoptosis proteins were assessed by western blot analysis. These results demonstrated that GRh2 and GRg3 inhibited cell growth and induced apoptosis, and that GRh2 had greater cytotoxicity than GRg3. GRh2 induced generation of more mitochondrial ROS compared with GRg3 in Jurkat cells; however, this effect was ameliorated by subsequent treatment with mitoTEMPO. Furthermore, excess mitochondrial ROS induced by GRh2 was more potent than GRg3 in inhibiting cell proliferation and reducing MMP. In addition, expression levels of apoptosis‑associated proteins were significantly increased in Jurkat cells treated with GRh2 than GRg3. In conclusion, these findings suggested that GRh2 and GRg3 induce mitochondrial-associated apoptosis by increasing mitochondrial ROS in human leukemia Jurkat cells. GRh2 may more effectively inhibit cell growth and accelerate apoptosis than GRg3. This study provides a potential novel strategy for the treatment of acute lymphoblastic leukemia.
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