ArticleNeuroscience bulletin2009
Effects of caffeic acid, rofecoxib, and their combination against quinolinic acid-induced behavioral alterations and disruption in glutathione redox status.
Article in Neuroscience bulletin, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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12 citing papers in PubMed, 21 citations in OpenAlex.
- Pathomechanisms of behavioral abnormalities in Huntington disease: an update.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- An Overview of the Pathophysiological Mechanisms of 3-Nitropropionic Acid (3-NPA) as a Neurotoxin in a Huntington's Disease Model and Its Relevance to Drug Discovery and Development.Neurochemical research · 2023Review
- Therapeutic Implications of Caffeic Acid in Cancer and Neurological Diseases.Frontiers in oncology · 2022Review
- Neuroprotective Effects of Coffee Bioactive Compounds: A Review.International journal of molecular sciences · 2020Review
- Anti-inflammatory activity of copao (Eulychnia acida Phil., Cactaceae) fruits.Plant foods for human nutrition (Dordrecht, Netherlands) · 2015Article
- A mitochondrial basis for Huntington's disease: therapeutic prospects.Molecular and cellular biochemistry · 2014Review
- Quinolinic acid: an endogenous neurotoxin with multiple targets.Oxidative medicine and cellular longevity · 2013Review
- Targeting neuro-inflammatory cytokines and oxidative stress by minocycline attenuates quinolinic-acid-induced Huntington's disease-like symptoms in rats.Neurotoxicity research · 2012Article
- Role of prostaglandins in neuroinflammatory and neurodegenerative diseases.Mediators of inflammation · 2012Review
- Role of LOX/COX pathways in 3-nitropropionic acid-induced Huntington's disease-like symptoms in rats: protective effect of licofelone.British journal of pharmacology · 2011Article
- Potential role of pioglitazone, caffeic acid and their combination against fatigue syndrome-induced behavioural, biochemical and mitochondrial alterations in mice.Inflammopharmacology · 2010Article
- 3-Nitropropionic acid as a tool to study the mechanisms involved in Huntington's disease: past, present and future.Molecules (Basel, Switzerland) · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveThe neuroprotective roles of cyclooxygenase (COX) and lipooxygenase (LOX) inhibitors have been well documented. Quinolinic acid (QA) is a well-known excitotoxic agent that could induce behavioral, morphological and biochemical alterations similar with symptoms of Huntington's disease (HD), by stimulating NMDA receptors. However, the exact roles of COX and LOX inhibitors in HD have not yet been explained. The present study aims to elucidate the effects of caffeic acid (a specific inhibitor for LOX), rofecoxib (a specific inhibitor for COX-2), and their combination in ameliorating QA-induced neurotoxicity in rats.
methodsQA was injected into the right striatum of rats to induce neurotoxicity. Caffeic acid and rofecoxib were then orally administered separately. In the combination study, caffeic acid and rofecoxib were administered together. After that, a series of behavioral assessments were conducted to determine the effects of caffeic acid and rofecoxib, respectively, and the co-effect of caffeic acid and rofecoxib, against QA-induced neurotoxicity.
resultsIntrastriatal QA administration (300 nmol) not only induced a significant reduction in body weight and motor incoordination, but also altered the redox status (decreased glutathione and increased oxidized glutathione level) in striatum, as compared to the sham group. Moreover, chronic treatment with caffeic acid (5 mg/kg and 10 mg/kg, respectively, p.o.) or rofecoxib (10 mg/kg, p.o.) could significantly attenuate QA-induced behavioral alterations and restore the redox status in striatum. However, at the dose of 2.5 mg/kg, caffeic acid did not show any significant effects on these parameters in QA-treated rats. Furthermore, the combination of rofecoxib (10 mg/kg) and caffeic acid (5 mg/kg) could significantly protect against QA neurotoxicity.
conclusionThe in vivo study indicates that excitotoxic injury to the brain might affect oxidant/antioxidant equilibrium by eliciting changes in glutathione. Moreover, the LOX and the COX pathways may be both involved in quinolinic-induced neurotoxicity, which provides a promising target for HD treatment.
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