Suppressing inflammatory cascade by cyclo-oxygenase inhibitors attenuates quinolinic acid induced Huntington's disease-like alterations in rats

Kalonia, Harikesh; Kumar, Anil

doi:10.1016/j.lfs.2011.02.020

Cited by 25 publications

(12 citation statements)

References 68 publications

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“…The intrastriatal QUIN administration induces a marked expression of tumor necrosis alpha (TNF- α ) [118] and interleukin-6 (IL-6) [119] that can be attenuated by inhibiting the cyclooxygenase 2 (COX-2) [120]. QUIN and TNF- α cause oligodendrocyte death by apoptotic process [121, 122].…”

Section: Inflammation and Quinmentioning

confidence: 99%

Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets

Lugo-Huitrón

Muñiz

Pineda

et al. 2013

Oxidative Medicine and Cellular Longevity

279

225

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Quinolinic acid (QUIN), a neuroactive metabolite of the kynurenine pathway, is normally presented in nanomolar concentrations in human brain and cerebrospinal fluid (CSF) and is often implicated in the pathogenesis of a variety of human neurological diseases. QUIN is an agonist of N-methyl-D-aspartate (NMDA) receptor, and it has a high in vivo potency as an excitotoxin. In fact, although QUIN has an uptake system, its neuronal degradation enzyme is rapidly saturated, and the rest of extracellular QUIN can continue stimulating the NMDA receptor. However, its toxicity cannot be fully explained by its activation of NMDA receptors it is likely that additional mechanisms may also be involved. In this review we describe some of the most relevant targets of QUIN neurotoxicity which involves presynaptic receptors, energetic dysfunction, oxidative stress, transcription factors, cytoskeletal disruption, behavior alterations, and cell death.

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Section: Inflammation and Quinmentioning

confidence: 99%

Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets

Lugo-Huitrón

Muñiz

Pineda

et al. 2013

Oxidative Medicine and Cellular Longevity

279

225

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“…For instance, chronic treatment with the selective cyclooxygenase- (COX-) 2 inhibitors celecoxib and meloxicam attenuated behavioral and biochemical changes in a quinolinic acid-induced rat model of HD [48]. Another study, however, failed to demonstrate positive effects of the nonselective COX inhibitor acetylsalicylate or the selective COX-2 inhibitor rofecoxib in N171-82Q and R6/2 HD transgenic mice [49].…”

Section: Anti-inflammatory Drugs For the Treatment Of Hdmentioning

confidence: 99%

Neuroimmunology of Huntington’s Disease: Revisiting Evidence from Human Studies

Rocha

Ribeiro

Furr-Stimming

et al. 2016

Mediators of Inflammation

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Huntington's disease (HD) is a neurodegenerative disorder characterized by selective loss of neurons in the striatum and cortex, which leads to progressive motor dysfunction, cognitive decline, and psychiatric disorders. Although the cause of HD is well described—HD is a genetic disorder caused by a trinucleotide (CAG) repeat expansion in the gene encoding for huntingtin (HTT) on chromosome 4p16.3—the ultimate cause of neuronal death is still uncertain. Apart from impairment in systems for handling abnormal proteins, other metabolic pathways and mechanisms might contribute to neurodegeneration and progression of HD. Among these, inflammation seems to play a role in HD pathogenesis. The current review summarizes the available evidence about immune and/or inflammatory changes in HD. HD is associated with increased inflammatory mediators in both the central nervous system and periphery. Accordingly, there have been some attempts to slow HD progression targeting the immune system.

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“…Chronic treatment with different COX inhibitors, such as rofecoxib, celecoxib, nimesulide, and meloxicam improved spontaneous locomotor activity and the motor performance, as well as these medicines reduced biochemical and mitochondrial alteration induced by QA [148–150]. Naproxen and valdecoxib, two COX inhibitors, also reduced 3-NP-induced motor and cognitive impairment [151].…”

Section: Roles Of Prostaglandins In Neurodegenerative Diseasesmentioning

confidence: 99%

Role of Prostaglandins in Neuroinflammatory and Neurodegenerative Diseases

Lima

Bastos

Limborço-Filho

et al. 2012

Mediators of Inflammation

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Increasing data demonstrates that inflammation participates in the pathophysiology of neurodegenerative diseases. Among the different inflammatory mediators involved, prostaglandins play an important role. The effects induced by prostaglandins might be mediated by activation of their known receptors or by nonclassical mechanisms. In the present paper, we discuss the evidences that link prostaglandins, as well as the enzymes that produce them, to some neurological diseases.

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Suppressing inflammatory cascade by cyclo-oxygenase inhibitors attenuates quinolinic acid induced Huntington's disease-like alterations in rats

Cited by 25 publications

References 68 publications

Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets

Quinolinic Acid: An Endogenous Neurotoxin with Multiple Targets

Neuroimmunology of Huntington’s Disease: Revisiting Evidence from Human Studies

Role of Prostaglandins in Neuroinflammatory and Neurodegenerative Diseases

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