ArticlePloS one2013
Edaravone protected human brain microvascular endothelial cells from methylglyoxal-induced injury by inhibiting AGEs/RAGE/oxidative stress.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 47 citations in OpenAlex.
- The Reductive Stress Nexus: Integrated Pathways of Metabolic Dysregulation, Senescence and Blood-Brain Barrier Failure in Neurodegenerative Disease and Brain Aging.Cell biochemistry and biophysics · 2026Review
- The interaction between dysfunction of vasculature and tauopathy in Alzheimer's disease and related dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Methylglyoxal, a highly reactive dicarbonyl compound, as a threat for blood brain barrier integrity.Fluids and barriers of the CNS · 2023Review
- Dicarbonyl Stress in Diabetic Vascular Disease.International journal of molecular sciences · 2022Review
- Methylglyoxal Scavengers Attenuate Angiogenesis Dysfunction Induced by Methylglyoxal and Oxygen-Glucose Deprivation.Oxidative medicine and cellular longevity · 2022Article
- The mFrontiers in endocrinology · 2022Article
- Article
- Inhibiting HMGB1-RAGE axis prevents pro-inflammatory macrophages/microglia polarization and affords neuroprotection after spinal cord injury.Journal of neuroinflammation · 2020Article
- Isosamidin fromAntioxidants (Basel, Switzerland) · 2020Article
- Dicarbonyl Stress and S-Glutathionylation in Cerebrovascular Diseases: A Focus on Cerebral Cavernous Malformations.Antioxidants (Basel, Switzerland) · 2020Review
- Edaravone Exerts Brain Protective Function by Reducing the Expression of AQP4, APP and Aβ Proteins.Open life sciences · 2019Article
- RAGE in the pathophysiology of skeletal muscle.Journal of cachexia, sarcopenia and muscle · 2018Review
- (-)-Epigallocatechin Gallate Inhibits Asymmetric Dimethylarginine-Induced Injury in Human Brain Microvascular Endothelial Cells.Neurochemical research · 2016Article
- Allicin prevents oxidized low-density lipoprotein-induced endothelial cell injury by inhibiting apoptosis and oxidative stress pathway.BMC complementary and alternative medicine · 2016Article
- Methylglyoxal induces mitochondrial dysfunction and cell death in liver.Toxicological research · 2014Article
- The receptor for advanced glycation end products (RAGE) specifically recognizes methylglyoxal-derived AGEs.Biochemistry · 2014Article
- Edaravone protects against methylglyoxal-induced barrier damage in human brain endothelial cells.PloS one · 2014Article
- Article
- Effects of methanolic extracts from edible plants on endogenous secretory receptor for advanced glycation end products induced by the high glucose incubation in human endothelial cells.Journal of pharmacy & bioallied sciencesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Subjects with diabetes experience an increased risk of cerebrovascular disease and stroke compared with nondiabetic age-matched individuals. Increased formation of reactive physiological dicarbonyl compound methylglyoxal (MGO) seems to be implicated in the development of diabetic vascular complication due to its protein glycation and oxidative stress effect. Edaravone, a novel radical scavenger, has been reported to display the advantageous effects on ischemic stroke both in animals and clinical trials; however, little is known about whether edaravone has protective effects on diabetic cerebrovascular injury. Using cultured human brain microvascular endothelial cells (HBMEC), protective effects of edaravone on MGO and MGO enhancing oxygen-glucose deprivation (OGD) induced injury were investigated. Cell injury was measured by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) formation, cell account, lactate dehydrogenase (LDH) release and Rhodamine 123 staining. Advanced glycation end-products (AGEs) formation and receptor for advanced glycation end-products (RAGE) expression were measured by western blotting. Cellular oxidative stress was measured by reactive oxygen species (ROS) release. Treatment of MGO for 24 h significantly induced HBMEC injury, which was inhibited by pretreatment of edaravone from 10-100 µmol/l. What's more, treatment of MGO enhanced AGEs accumulation, RAGE expression and ROS release in the cultured HBMEC, which were inhibited by 100 µmol/l edaravone. Finally, treatment of MGO for 24 h and then followed by 3 h OGD insult significantly enhanced cell injury when compared with OGD insult only, which was also protected by 100 µmol/l edaravone. Thus, edaravone protected HBMEC from MGO and MGO enhancing OGD-induced injury by inhibiting AGEs/RAGE/oxidative stress.
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