ArticleInternational journal of molecular sciences2018
Ginsenoside Rg1 Prevents Doxorubicin-Induced Cardiotoxicity through the Inhibition of Autophagy and Endoplasmic Reticulum Stress in Mice.
Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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Who cites it
58 citing papers in PubMed, 126 citations in OpenAlex.
- Interfacial and Molecular Mechanisms of Pancreatic Lipase Modulation by Saponin-Rich Extracts with Antioxidant Activity.Molecules (Basel, Switzerland) · 2026Article
- Research Progress on the Role of Traditional Chinese Medicine in Regulating Ferroptosis in Cardiovascular Diseases.Biology · 2026Review
- Research progress of ginseng active ingredients combined with chemotherapy in cancer therapy.Journal of ginseng research · 2026Review
- Protective Effects of Ginsenosides on Drug-induced Cardiotoxicity: A New Therapeutic Approach with Focus on Molecular Mechanisms in Cardio-oncology Field.Current medicinal chemistry · 2026Review
- Article
- Astaxanthin mitigates cardiac toxicity induced via doxorubicin by alleviating mitochondrial fission and autophagy in rats.Scientific reports · 2025Article
- Therapeutic Potential of Ginsenosides in Anthracycline-Induced Cardiotoxicity.Molecules (Basel, Switzerland) · 2025Review
- Advances in pharmacological research on myocardial remodeling agents: A decade in review.Medicine · 2025Review
- Unveiling the Complexities: Exploring Mechanisms of Anthracyclineinduced Cardiotoxicity.Current cardiology reviews · 2025Review
- Natural Products From Traditional Chinese Medicine: Potential Therapeutic Agents in Cancer Therapy-Induced Cardiotoxicity.Drug design, development and therapy · 2025Review
- A review of cardioprotective effect of ginsenosides in chemotherapy-induced cardiotoxicity.Biomedical engineering online · 2024Review
- Article
- Momordica charantia L.-derived exosome-like nanovesicles stabilize p62 expression to ameliorate doxorubicin cardiotoxicity.Journal of nanobiotechnology · 2024Article
- Precision Treatment of Anthracycline-Induced Cardiotoxicity: An Updated Review.Current treatment options in oncology · 2024Review
- Natural Products for Preventing and Managing Anthracycline-Induced Cardiotoxicity: A Comprehensive Review.Cells · 2024Review
- Red ginseng prevents doxorubicin-induced cardiomyopathy by inhibiting cell death via activating the Nrf2 pathway.Cardio-oncology (London, England) · 2024Article
- Exploring Anthracycline-Induced Cardiotoxicity from the Perspective of Protein Quality Control.Reviews in cardiovascular medicine · 2024Review
- Mass Production of Rg1-Loaded Small Extracellular Vesicles Using a 3D Bioreactor System for Enhanced Cardioprotective Efficacy of Doxorubicin-Induced Cardiotoxicity.Pharmaceutics · 2024Article
- Anti-leukemia effects of ginsenoside monomer: A narrative review of pharmacodynamics study.Current therapeutic research, clinical and experimental · 2024Review
- A review of chemotherapeutic drugs-induced arrhythmia and potential intervention with traditional Chinese medicines.Frontiers in pharmacology · 2024Review
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5 authors at 1 institution in 1 country.
Funding
Abstract
Ginsenoside Rg1, a saponin that is a primary component of ginseng, has been demonstrated to protect hearts from diverse cardiovascular diseases with regulating multiple cellular signal pathways. In the present study, we investigated the protective role of ginsenoside Rg1 on doxorubicin-induced cardiotoxicity and its effects on endoplasmic reticulum stress and autophagy. After pre-treatment with ginsenoside Rg1 (50 mg/kg i.g.) for 7 days, male C57BL/6J mice were intraperitoneally injected with a single dose of doxorubicin (6 mg/kg) every 3 days for four injections. Echocardiographic and pathological findings showed that ginsenoside Rg1 could significantly reduce the cardiotoxicity induced by doxorubicin. Ginsenoside Rg1 significantly inhibited doxorubicin-induced formation of autophagosome. At the same time, ginsenoside Rg1 decreased the doxorubicin-induced cardiac microtubule-associated protein-light chain 3 and autophagy related 5 expression. Ginsenoside Rg1 can reduce endoplasmic reticulum dilation caused by doxorubicin. Compared with the doxorubicin group, the expression of cleaved activating transcription factor 6 and inositol-requiring enzyme 1 decreased in group ginsenoside Rg1. Treatment with ginsenoside Rg1 reduces the expression of TIF1 and increases the expression of glucose-regulated protein 78. In the ginsenoside Rg1 group, the expression of p-P70S6K, c-Jun N-terminal kinases 1 and Beclin1 declined. These results indicate that ginsenoside Rg1 may improve doxorubicin-induced cardiac dysfunction by inhibiting endoplasmic reticulum stress and autophagy.
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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.