ArticleMolecular biology reports2020
Melatonin and vitamin E alleviate homocysteine-induced oxidative injury and apoptosis in endothelial cells.
Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Melatonin and Vitamins: A Promising Combination to Augment Conventional Anticancer Therapies.Nutrients · 2025Review
- Homocysteine Attack on Vascular Endothelium-Old and New Features.International journal of molecular sciences · 2025Review
- Melatonin Interplay in Physiology and Disease-The Fountain of Eternal Youth Revisited.Biomolecules · 2025Review
- Intracellular Iron Deficiency and Abnormal Metabolism, Not Ferroptosis, Contributes to Homocysteine-Induced Vascular Endothelial Cell Death.Biomedicines · 2024Article
- Article
- Melatonin and Vascular Function.Antioxidants (Basel, Switzerland) · 2024Review
- Effects of N-acetylcysteine on CG8005 gene-mediated proliferation and apoptosis of Drosophila S2 embryonic cells.Scientific reports · 2023Article
- Review
- Effect of melatonin on electrical impedance and biomarkers of damage in a gastric ischemia/reperfusion model.PloS one · 2022Article
- Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis.Frontiers in cardiovascular medicine · 2022Review
- Melatonin as a Reducer of Neuro- and Vasculotoxic Oxidative Stress Induced by Homocysteine.Antioxidants (Basel, Switzerland) · 2021Review
- Toxicology of Blister Agents: Is Melatonin a Potential Therapeutic Option?Diseases (Basel, Switzerland) · 2021Review
- Homocysteine in Neurology: A Possible Contributing Factor to Small Vessel Disease.International journal of molecular sciences · 2021Review
- Melatonin Alleviates the Toxicity of High Nicotinamide Concentrations in Oocytes: Potential Interaction with Nicotinamide Methylation Signaling.Oxidative medicine and cellular longevity · 2021Article
- Quercetin, chrysin, caffeic acid and ferulic acid ameliorate cyclophosphamide-induced toxicities in SH-SY5Y cells.Molecular biology reports · 2020Article
- CG8005 Mediates Transit-Amplifying Spermatogonial Divisions via Oxidative Stress inOxidative medicine and cellular longevity · 2020Article
- Hyperhomocysteinemia: Clinical Insights.Journal of central nervous system disease · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
A relationship exists between hyperhomocysteinemia and cardiovascular diseases, although the underlying mechanisms are still incompletely defined. One possibility involves a homocysteine (Hcy)-induced increased oxidative stress. Melatonin (Mel) and vitamin E (vitE) are important anti-oxidants. The main purpose of this study was (1) to compare the effect of treatments with Mel, vitE or both, on Hcy-induced apoptosis in human umbilical vein endothelial cells (HUVECs), and (2) to investigate the underlying mechanisms. Cell proliferation assay was carried out by Water Soluble Tetrazolium-1 (WST-1) assay kit. Apoptotic index was calculated by TUNEL Assay. Anti-oxidant parameters were studied by measurement of reactive oxygen species (ROS) and lipid peroxidation (LPO) levels. mRNA and protein expression levels of apoptotic and anti-apoptotic genes and proteins were studied by quantitative real time polymerase chain reaction (qRT-PCR) and Western blotting experiments respectively. The results showed that treatments with Mel, vitE or Mel + vitE suppressed Hcy-induced cell death, with a higher efficiency for the Mel and Mel + vitE treatments. Our results suggests that the mechanisms by which these anti-oxidants protected endothelial cells include the decrease in ROS and LPO levels, an increase in cell migration, the downregulation of pro-apoptotic proteins Cas 3, Cas 9, Cyt C and Bax and the upregulation of anti-apoptotic protein Bcl 2. Collectively, these results revealed the protective role of vitE and Mel against Hcy-induced cell apoptosis, which may add insight into therapeutic approaches to Hcy-induced damages.
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Registered trials
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