ArticleActa Cardiologica Sinica2018
Melatonin Protects Against Hypoxia/Reoxygenation-Induced Dysfunction of Human Umbilical Vein Endothelial Cells Through Inhibiting Reactive Oxygen Species Generation.
Article in Acta Cardiologica Sinica, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Exploring melatonin's multifaceted role in female reproductive health: From follicular development to lactation and its therapeutic potential in obstetric syndromes.Journal of advanced research · 2025Review
- Melatonin-Mediated Suppression of mtROS-JNK-FOXO1 Pathway Alleviates Hypoxia-Induced Apoptosis in Porcine Granulosa Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Melatonin attenuates high glucose‑induced endothelial cell pyroptosis by activating the Nrf2 pathway to inhibit NLRP3 inflammasome activation.Molecular medicine reports · 2023Article
- Effect of melatonin on electrical impedance and biomarkers of damage in a gastric ischemia/reperfusion model.PloS one · 2022Article
- Melatonin for the Management of Preeclampsia: A Review.Antioxidants (Basel, Switzerland) · 2021Review
- Melatonin Alleviates Hypoxia-Induced Apoptosis of Granulosa Cells by Reducing ROS and Activating MTNR1B-PKA-Caspase8/9 Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Inhibition of miR-214-3p Protects Endothelial Cells from ox-LDL-Induced Damage by Targeting GPX4.BioMed research international · 2021Article
- Beneficial Effects of Hydroalcoholic Extract fromActa Cardiologica Sinica · 2020Article
- Protective Roles and Mechanisms of Taurine on Myocardial Hypoxia/Reoxygenation-Induced Apoptosis.Acta Cardiologica Sinica · 2019Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundHypoxia/reoxygenation (H/R) in human umbilical vein endothelial cells (HUVECs) induces oxidative stress and eventually leads to vascular injury.
objectiveThe aim of this study was to examine the effect of melatonin on HUVECs injured by H/R and explore the underlying mechanisms. MATERIALS AND
methodsA model of HUVECs under hypoxia/reoxygenation was established. Cell migration and adhesive ability was measured by wound healing and adhesion assays. Cell proliferation was measured by EdU assay. Production of reactive oxygen species (ROS) was evaluated by CM-H
resultsH/R inhibited HUVEC proliferation, cell migratory and adhesive capacities, whereas melatonin (1~100 μM) inhibited these effects in a dose-dependent manner. Melatonin alone did not affect HUVEC viability, however, it inhibited the increase in ROS production and cytoskeleton disruption elicited by H/R, and it dose-dependently prevented H/R-induced upregulation of P38 and HSP27 phosphorylation. In addition, the ROS scavenger N-acetyl-L-cysteine markedly inhibited increased phosphorylation levels of P38 and HSP27 under H/R.
conclusionsMelatonin may have a potential clinical effect in trials of H/R-induced vascular injury through its antioxidant property.
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