Background/aim: We investigated the effects of chloroquine, an autophagy inhibitor, on doxorubicin-induced apoptosis in A549 cells.
Materials And Methods: A549 cells were treated with doxorubicin, chloroquine, or both. Then, cytotoxicity was measured. The expression levels of caspases and mitogen-activated protein kinases were also quantified. In addition, the levels of doxorubicin-derived reactive oxygen species were measured.
Results: Chloroquine enhanced doxorubicin-induced apoptosis and oxidative stress and suppressed the doxorubicin-induced extracellular-signal-regulated kinase activation.
Conclusion: Chloroquine enhances doxorubicin-induced and oxidative stress-mediated apoptosis. This mechanism may involve the dephosphorylation of extracellular-signal-regulated kinases.
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http://dx.doi.org/10.21873/anticanres.15899 | DOI Listing |
Toxicol Rep
June 2025
Therapeutic Chemistry Department, Pharmaceutical and Drug Industries Research Institute, National Research Centre, El Buhouth St., Dokki, Cairo 12622, Egypt.
Doxorubicin (DOX) is a powerful antineoplastic FDA-approved anthracycline-derived antibiotic and is considered as the most suitable intervention for solid tumors and hematological cancers therapy. However, its therapeutic application is highly limited due to acute and chronic renal, hematological and testicular toxicity. Oxidative stress, lipid peroxidation and apoptosis in germ cells as well as low sperm count, motility and disturbing steroidogenesis are the principal machineries of DOX-induced testicular toxicity.
View Article and Find Full Text PDFCardiovasc Drugs Ther
January 2025
Department of Pharmacy, The Second Xiangya Hospital, Central South University, Changsha, 410011, Hunan, China.
Purpose: Doxorubicin (Dox) is a classic anthracycline chemotherapy drug with cause cumulative and dose-dependent cardiotoxicity. This study aimed to investigate the potential role and molecular mechanism of phenylacetylglutamine (PAGln), a novel gut microbiota metabolite, in Dox-induced cardiotoxicity (DIC).
Methods: DIC models were established in vivo and in vitro, and a series of experiments were performed to verify the cardioprotective effect of PAGln.
RSC Adv
January 2025
Tianjin Key Laboratory for Modern Drug Delivery and High-Efficiency, School of Pharmaceutical Science and Technology, Tianjin University Weijin Road Tianjin 300072 China +86-22-87401895 +86-22-87401895.
[This retracts the article DOI: 10.1039/C8RA07163B.].
View Article and Find Full Text PDFAppl Biochem Biotechnol
January 2025
Department of Pharmacology, Faculty of Veterinary Medicine, Assiut University, Assiut, 71516, Egypt.
Doxorubicin (DOX) is a commonly used chemotherapeutic medication for treating malignancies, although its cardiotoxicity limits its use. There is growing evidence that alteration of the mitochondrial fission/fusion dynamic processes accompanied by excessive reactive oxygen species (ROS) production and alteration of calcium Ca homeostasis are potential underlying mechanisms of DOX-induced cardiotoxicity (DIC). Metformin (Met) is an AMP-activated protein kinase (AMPK) activator that has antioxidant properties and cardioprotective effects.
View Article and Find Full Text PDFJ Cell Mol Med
January 2025
Zhengzhou Key Laboratory of Cardiovascular Aging, Henan Province Key Laboratory for Prevention and Treatment of Coronary Heart Disease, National Health Commission key Laboratory of Cardiovascular Regenerative Medicine, Central China Fuwai Hospital of Zhengzhou University, Fuwai Central China Cardiovascular Hospital & Central China Branch of National Center for Cardiovascular Diseases, Zhengzhou, Henan, China.
N6-adenosine methylation (m6A) of RNA is involved in the regulation of various diseases. However, its role in chemotherapy-related vascular endothelial injury has not yet been elucidated. We found that methyltransferase-like 3 (METTL3) expression was significantly reduced during doxorubicin (DOX)-induced apoptosis of vascular endothelial cells both in vivo and in vitro, and that silencing of METTL3 further intensified this process.
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