ArticleLaboratory animal research2011
Esculetin inhibits N-methyl-D-aspartate neurotoxicity via glutathione preservation in primary cortical cultures.
Article in Laboratory animal research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Unlocking the Potential ofBiology · 2026Review
- Esculetin attenuates migraine-like pain via CGRP suppression and meningeal mast cell modulation in rat models.Journal of Zhejiang University. Science. B · 2026Article
- The Role of Coumarins in Drug Discovery: Pharmacological Insights and Structural Innovations.Current topics in medicinal chemistry · 2026Review
- Antioxidant and anti‑inflammatory effects of esculin and esculetin (Review).Experimental and therapeutic medicine · 2024Review
- Esculetin Alleviates IL-1β-Evoked Nucleus Pulposus Cell Death, Extracellular Matrix Remodeling, and Inflammation by Activating Nrf2/HO-1/NF-kb.ACS omega · 2024Article
- Therapeutic Effects of Coumarins with Different Substitution Patterns.Molecules (Basel, Switzerland) · 2023Review
- Natural Coumarins: Exploring the Pharmacological Complexity and Underlying Molecular Mechanisms.Oxidative medicine and cellular longevity · 2021Review
- Review
- Esculetin as a Bifunctional Antioxidant Prevents and Counteracts the Oxidative Stress and Neuronal Death Induced by Amyloid Protein in SH-SY5Y Cells.Antioxidants (Basel, Switzerland) · 2020Article
- Antimicrobial Activities of Extracts and Isolated Coumarins from the Roots of FourIranian journal of pharmaceutical research : IJPR · 2019Article
- The α-amylase and α-glucosidase inhibitory activities of the dichloromethane extracts and constituents of Ferulago bracteata roots.Pharmaceutical biology · 2018Article
- Prostaglandin actions in established insect cell lines.In vitro cellular & developmental biology. Animal · 2017Article
- Urtica dioica leaves modulates muscarinic cholinergic system in the hippocampus of streptozotocin-induced diabetic mice.Metabolic brain disease · 2015Article
- Review on natural coumarin lead compounds for their pharmacological activity.BioMed research international · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recently, loss of endogenous glutathione during N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxic injury, and the resultant overproduction of reactive oxygen species (ROS) through an arachidonic acid cascade process in brain, have been implicated in neuronal damage in various neurodegenerative diseases. Glutathione depletion induced by L-buthionine-(S,R)-sulfoximine (BSO), an inhibitor of glutathione synthesis, is known to cause arachidonic acid-mediated excitotoxicity in primary mixed cortical cultures. The aim of this study was to investigate whether esculetin (6,7-dihydroxycoumarin), an inhibitor of lipoxygenase, protects against neurotoxicity induced by NMDA or BSO. We observed that neurotoxicity induced by NMDA but not kainic acid was attenuated by esculetin. At the same concentration (100 µM), esculetin attenuated the (45)Ca(2+) uptake elevation induced by NMDA. Free radical-mediated neuronal injury induced by H(2)O(2) and xanthine/xanthine oxidase was concentration-dependently blocked by esculetin. Esculetin (1-30 µM) dose-dependently inhibited BSO-induced neuronal injury. In addition, arachidonate-induced neurotoxicity was completely blocked by esculetin. BSO also reduced glutathione peroxidase (GPx) activity, but did not change glutathione reductase (GR) activity 24 h after treatment. Esculetin dose-dependently increased GR activity, but did not alter GPx activity. These findings suggest that esculetin can contribute to the rescue of neuronal cells from NMDA neurotoxicity and that this protective effect occurs partly through NMDA receptor modulation and the sparing of glutathione depletion.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.