naphthoquinones has been researched along with Cardiotoxicity* in 3 studies
3 other study(ies) available for naphthoquinones and Cardiotoxicity
| Article | Year |
|---|---|
β-LAPachone ameliorates doxorubicin-induced cardiotoxicity via regulating autophagy and Nrf2 signalling pathways in mice.
Topics: AMP-Activated Protein Kinases; Animals; Antibiotics, Antineoplastic; Antioxidants; Autophagy; Cardiotoxicity; Cell Survival; Doxorubicin; Malondialdehyde; Mice; Mice, Inbred C57BL; Naphthoquinones; NF-E2-Related Factor 2; Oxidative Stress; Signal Transduction | 2020 |
Plumbagin protects the myocardial damage by modulating the cardiac biomarkers, antioxidants, and apoptosis signaling in the doxorubicin-induced cardiotoxicity in rats.
Cardiovascular disease created enormous health and economic burdens worldwide, which is responsible for the highest mobility and mortality that results in nearly 6.2% of in-hospital deaths every year. Plumbagin is a major bioactive compound that occurs in the Plumbago indica and P. zeylanica with numerous therapeutic benefits. The current research exploration was planned to investigate the therapeutic role of plumbagin against doxorubicin stimulated cardiotoxicity in rats. The cardiotoxicity was stimulated to the rats by administering the 2.5 mg/kg of doxorubicin for 14 days with concurrent supplementation with plumbagin. The hemodynamic parameters were studied by using the tail-cuff plethysmography. The lipid peroxidation and antioxidant status was examined by the standard procedures. The myocardial function and damage markers were assessed with the help of commercial kits. The expression status of inflammatory markers and PI3K/Akt signaling markers were investigated by reverse transcription polymerase chain reaction (RT-PCR) and western blotting analysis, respectively. The plumbagin supplementation appreciably regained the body weight and heart weight of the investigational animals. Hemodynamic parameters and antioxidants statuses were escalated by the plumbagin treatment. The severe elevation in the cardiac damage markers and inflammatory markers were noticeably ameliorated by the plumbagin treatment. The plumbagin treatment also assuaged the overexpression of inflammatory and apoptotic proteins in the heart tissues of doxorubicin-challenged rats. The histopathological analysis revealed that the plumbagin appreciably protected the heart tissues from the doxorubicin-induced damages. The findings of this exploration evidenced that plumbagin treatment attenuated the doxorubicin-stimulated cardiotoxicity in rats. Topics: Animals; Antioxidants; Apoptosis; Apoptosis Regulatory Proteins; Biomarkers; Cardiotoxicity; Cytokines; Doxorubicin; Heart; Lipid Peroxidation; Male; Myocardium; Naphthoquinones; Phosphatidylinositol 3-Kinases; Rats; Rats, Wistar; Signal Transduction | 2020 |
Spinochrome D Attenuates Doxorubicin-Induced Cardiomyocyte Death via Improving Glutathione Metabolism and Attenuating Oxidative Stress.
Doxorubicin, an anthracycline from Topics: Animals; Antibiotics, Antineoplastic; Apoptosis; Cardiotonic Agents; Cardiotoxicity; Cell Survival; Doxorubicin; Female; Glutathione; HeLa Cells; Humans; MCF-7 Cells; Membrane Potential, Mitochondrial; Metabolomics; Mitochondria; Myocytes, Cardiac; Naphthoquinones; Neoplasms; Nuclear Magnetic Resonance, Biomolecular; Oxidative Stress; Proteomics; Proton Magnetic Resonance Spectroscopy; Rats; Reactive Oxygen Species; Sea Urchins | 2018 |