ArticleCell proliferation2014
Quercetin ameliorates tunicamycin-induced endoplasmic reticulum stress in endothelial cells.
Article in Cell proliferation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 76 citations in OpenAlex.
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- Treatment of T2DM-related inflammation and vascular injury by regulating cellular crosstalk in the islet microenvironment.Frontiers in endocrinology · 2025Review
- Decoding interaction between mitochondria and endoplasmic reticulum in ischemic myocardial injury: targeting natural medicines.Frontiers in pharmacology · 2025Review
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- Potential of natural drug modulation of endoplasmic reticulum stress in the treatment of myocardial injury.Journal of pharmaceutical analysis · 2024Review
- The protective role of selenium against high-fructose corn syrup-induced kidney damage: a histopathological and molecular analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Quantitative proteomic analyses uncover regulatory roles of Nrf2 in human endothelial cells.Cell stress & chaperones · 2023Article
- Selected Plant-Derived Polyphenols as Potential Therapeutic Agents for Peripheral Artery Disease: Molecular Mechanisms, Efficacy and Safety.Molecules (Basel, Switzerland) · 2022Review
- Tunicamycin-Induced Endoplasmic Reticulum Stress Damages Complex I in Cardiac Mitochondria.Life (Basel, Switzerland) · 2022Article
- Quercetin ameliorates testosterone secretion disorder by inhibiting endoplasmic reticulum stress through the miR-1306-5p/HSD17B7 axis in diabetic rats.Bosnian journal of basic medical sciences · 2022Article
- Quercetin Alleviates Endoplasmic Reticulum Stress-Induced Apoptosis in Buffalo Ovarian Granulosa Cells.Animals : an open access journal from MDPI · 2022Article
- Protective and therapeutic role of melatonin against tunicamycin-induced ER stress in testicular tissue of rats.Iranian journal of basic medical sciences · 2022Article
- Vascular Protective Effect and Its Possible Mechanism of Action on Selected Active Phytocompounds: A Review.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Oleoylethanolamide Alleviates Hepatic Ischemia-Reperfusion Injury via Inhibiting Endoplasmic Reticulum Stress-Associated Apoptosis.PPAR research · 2022Article
- An Endoplasmic Reticulum-Targeted Ratiometric Fluorescent Molecule Reveals ZnFrontiers in pharmacology · 2022Article
- Targeting Oxidative Phosphorylation-Proteasome Activity in Extracellular Detached Cells Promotes Anoikis and Inhibits Metastasis.Life (Basel, Switzerland) · 2021Article
- Endoplasmic reticulum stress as the basis of obesity and metabolic diseases: focus on adipose tissue, liver, and pancreas.European journal of nutrition · 2021Review
- Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases.Nature reviews. Cardiology · 2021Review
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveEndothelial dysfunction highlights that it is a potential contributor in the pathogenesis of vascular complications arising from endoplasmic reticulum stress (ER stress) and has been emerging as a main causative factor in vascular failure. Here, we hypothesize that the natural flavonoid, quercetin plays an effective role in reducing ER stress in human umbilical vein endothelial cells. MATERIALS AND
methodsHuman umbilical vein endothelial cells were pre-treated with different concentrations of quercetin (0-100 μm) before inducing ER stress using tunicamycin (TUN) (0.75 μg/ml); cytotoxicity was assessed by MTT assay. Expression levels of ER stress responsive genes, antioxidant enzymes and apoptotic markers were assessed by qRT-PCR, while roles of caspase-3 and PARP cleavage were measured by western blot analysis.
resultsQuercetin pre-treatment at 25 and 50 μm had a cytoprotective effect on cells against TUN-induced toxicity. Quercetin administration modulated expression level of ER stress genes coding for glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP), and antioxidant enzymes such as superoxide dismutase and catalase, along with free radical generation assessed by malondialdehyde assay. Induction of apoptosis was prevented with reduction in expression level of Bax, and concomitant increase in Bcl-2 levels, thus proving its potential against ER stress.
conclusionThe current study indicates that quercetin modulated stress responsive genes GRP78 and CHOP, helping endothelial cells prevent TUN-induced ER stress.
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