About: Tempol ameliorates murine viral encephalomyelitis by preserving the blood–brain barrier, reducing viral load, and lessening inflammation

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About: Tempol ameliorates murine viral encephalomyelitis by preserving the blood–brain barrier, reducing viral load, and lessening inflammation Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Tempol ameliorates murine viral encephalomyelitis by preserving the blood–brain barrier, reducing viral load, and lessening inflammation
Creator	Augusto, Ohara Linares, Edlaine Chadi, Gerson Giorgio, Selma Pereira, Carlos Tsuhako, Maria
Source	Elsevier; Medline; PMC
abstract	Abstract Multiple sclerosis (MS) is a progressive inflammatory and/or demyelinating disease of the human central nervous system (CNS). Most of the knowledge about the pathogenesis of MS has been derived from murine models, such as experimental autoimmune encephalomyelitis and viral encephalomyelitis. Here, we infected female C57BL/6 mice with a neurotropic strain of the mouse hepatitis virus (MHV-59A) to evaluate whether treatment with the multifunctional antioxidant tempol (4-hydroxy-2,2,6,6-tetramethyl-1-piperidinyloxy) affects the ensuing encephalomyelitis. In untreated animals, neurological symptoms developed quickly: 90% of infected mice died 10 days after virus inoculation and the few survivors presented neurological deficits. Treatment with tempol (24 mg/kg, ip, two doses on the first day and daily doses for 7 days plus 2 mM tempol in the drinking water ad libitum) profoundly altered the disease outcome: neurological symptoms were attenuated, mouse survival increased up to 70%, and half of the survivors behaved as normal mice. Not surprisingly, tempol substantially preserved the integrity of the CNS, including the blood–brain barrier. Furthermore, treatment with tempol decreased CNS viral titers, macrophage and T lymphocyte infiltration, and levels of markers of inflammation, such as expression of inducible nitric oxide synthase, transcription of tumor necrosis factor-α and interferon-γ, and protein nitration. The results indicate that tempol ameliorates murine viral encephalomyelitis by altering the redox status of the infectious environment that contributes to an attenuated CNS inflammatory response. Overall, our study supports the development of therapeutic strategies based on nitroxides to manage neuroinflammatory diseases, including MS.
has issue date	2010-03-01(xsd:dateTime)
bibo:doi	10.1016/j.freeradbiomed.2009.12.013
bibo:pmid	20035861
has license	els-covid
sha1sum (hex)	40bcf4faf38ac363d4f0a5e22a290976b18af0f0
schema:url	https://doi.org/10.1016/j.freeradbiomed.2009.12.013
resource representing a document's title	Tempol ameliorates murine viral encephalomyelitis by preserving the blood–brain barrier, reducing viral load, and lessening inflammation
has PubMed Central identifier	PMC7126783
has PubMed identifier	20035861
schema:publication	Free Radical Biology and Medicine
resource representing a document's body	covid:40bcf4faf38ac363d4f0a5e22a290976b18af0f0#body_text
is schema:about of	named entity 'supports' named entity 'virus' named entity 'mice' named entity 'mice' named entity 'Multiple sclerosis' named entity 'survivors' named entity 'CNS' named entity 'INCREASED' named entity 'HUMAN' named entity 'DAY' named entity 'REDUCING' named entity 'VIRAL LOAD' named entity 'VIRAL' named entity 'DISEASES' named entity 'STRATEGIES' named entity 'MS.' named entity 'DISEASE OUTCOME' named entity 'MANAGE' named entity 'INFLAMMATORY RESPONSE' named entity 'DEVELOPMENT' named entity '90%' named entity 'UNTREATED' named entity 'PROTEIN ' named entity '70%' named entity 'MACROPHAGE' named entity 'INTERFERON' named entity 'T LYMPHOCYTE' named entity 'MICE' named entity '59A' named entity 'HERE' named entity 'AMELIORATES' named entity 'NITROXIDES' named entity '2 MM' named entity 'INFLAMMATION' named entity 'FEMALE' named entity 'NEUROTROPIC' named entity 'C57BL' named entity 'ALTERED' named entity 'REDOX' named entity 'DECREASED' named entity 'TUMOR NECROSIS FACTOR' named entity 'DERIVED' named entity 'VIRAL' named entity 'TEMPOL' named entity 'INCLUDING' named entity 'OVERALL' named entity 'EXPRESSION' named entity 'LEVELS' named entity 'BLOOD-BRAIN BARRIER' named entity 'SURVIVAL' named entity 'NEUROLOGICAL' named entity 'IS A' named entity 'CENTRAL NERVOUS SYSTEM' named entity 'MARKERS' named entity 'MURINE' named entity 'TEMPOL' named entity 'ENCEPHALOMYELITIS' named entity 'MURINE' named entity 'VIRUS' named entity 'MULTIPLE SCLEROSIS' named entity 'TRANSCRIPTION' named entity 'INFLAMMATORY' named entity 'HALF' named entity 'CNS' named entity 'MOUSE HEPATITIS VIRUS' named entity 'AMELIORATES' named entity 'INFLAMMATION' named entity 'AD LIBITUM' named entity 'NEUROLOGICAL SYMPTOMS' named entity 'INDUCIBLE NITRIC OXIDE SYNTHASE' named entity 'ANTIOXIDANT' named entity 'MOST OF' named entity 'DRINKING WATER' named entity 'PRESERVING' named entity 'DAYS' named entity 'DOSES'

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