Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.

<h4>Background</h4>Ischemic brain injury is associated with neuroinflammatory response, which essentially involves glial activation and neutrophil infiltration. Transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) contribute to is...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Lu Yu, Chu Chen, Liang-Fen Wang, Xi Kuang, Ke Liu, Hao Zhang, Jun-Rong Du
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/e19cbb7e890c4af0b0c008a89ea3c79a
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:e19cbb7e890c4af0b0c008a89ea3c79a
record_format	dspace
spelling	oai:doaj.org-article:e19cbb7e890c4af0b0c008a89ea3c79a2021-11-18T07:56:59ZNeuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.1932-620310.1371/journal.pone.0055839https://doaj.org/article/e19cbb7e890c4af0b0c008a89ea3c79a2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23437066/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Ischemic brain injury is associated with neuroinflammatory response, which essentially involves glial activation and neutrophil infiltration. Transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) contribute to ischemic neuroinflammatory processes and secondary brain injury by releasing proinflammatory mediators. Kaempferol-3-O-rutinoside (KRS) and kaempferol-3-O- glucoside (KGS) are primary flavonoids found in Carthamus tinctorius L. Recent studies demonstrated that KRS protected against ischemic brain injury. However, little is known about the underlying mechanisms. Flavonoids have been reported to have antiinflammatory properties. Herein, we explored the effects of KRS and KGS in a transient focal stroke model.<h4>Methodology/principal findings</h4>Rats were subjected to middle cerebral artery occlusion for 2 hours followed by 22 h reperfusion. An equimolar dose of KRS or KGS was administered i.v. at the beginning of reperfusion. The results showed that KRS or KGS significantly attenuated the neurological deficits, brain infarct volume, and neuron and axon injury, reflected by the upregulation of neuronal nuclear antigen-positive neurons and downregulation of amyloid precursor protein immunoreactivity in the ipsilateral ischemic hemisphere. Moreover, KRS and KGS inhibited the expression of OX-42, glial fibrillary acidic protein, phosphorylated STAT3 and NF-κB p65, and the nuclear content of NF-κB p65. Subsequently, these flavonoids inhibited the expression of tumor necrosis factor α, interleukin 1β, intercellular adhesion molecule 1, matrix metallopeptidase 9, inducible nitric oxide synthase, and myeloperoxidase.<h4>Conclusion/significance</h4>Our findings suggest that postischemic treatment with KRS or KGS prevents ischemic brain injury and neuroinflammation by inhibition of STAT3 and NF-κB activation and has the therapeutic potential for the neuroinflammation-related diseases, such as ischemic stroke.Lu YuChu ChenLiang-Fen WangXi KuangKe LiuHao ZhangJun-Rong DuPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 2, p e55839 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lu Yu Chu Chen Liang-Fen Wang Xi Kuang Ke Liu Hao Zhang Jun-Rong Du Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.
description	<h4>Background</h4>Ischemic brain injury is associated with neuroinflammatory response, which essentially involves glial activation and neutrophil infiltration. Transcription factors nuclear factor-κB (NF-κB) and signal transducer and activator of transcription 3 (STAT3) contribute to ischemic neuroinflammatory processes and secondary brain injury by releasing proinflammatory mediators. Kaempferol-3-O-rutinoside (KRS) and kaempferol-3-O- glucoside (KGS) are primary flavonoids found in Carthamus tinctorius L. Recent studies demonstrated that KRS protected against ischemic brain injury. However, little is known about the underlying mechanisms. Flavonoids have been reported to have antiinflammatory properties. Herein, we explored the effects of KRS and KGS in a transient focal stroke model.<h4>Methodology/principal findings</h4>Rats were subjected to middle cerebral artery occlusion for 2 hours followed by 22 h reperfusion. An equimolar dose of KRS or KGS was administered i.v. at the beginning of reperfusion. The results showed that KRS or KGS significantly attenuated the neurological deficits, brain infarct volume, and neuron and axon injury, reflected by the upregulation of neuronal nuclear antigen-positive neurons and downregulation of amyloid precursor protein immunoreactivity in the ipsilateral ischemic hemisphere. Moreover, KRS and KGS inhibited the expression of OX-42, glial fibrillary acidic protein, phosphorylated STAT3 and NF-κB p65, and the nuclear content of NF-κB p65. Subsequently, these flavonoids inhibited the expression of tumor necrosis factor α, interleukin 1β, intercellular adhesion molecule 1, matrix metallopeptidase 9, inducible nitric oxide synthase, and myeloperoxidase.<h4>Conclusion/significance</h4>Our findings suggest that postischemic treatment with KRS or KGS prevents ischemic brain injury and neuroinflammation by inhibition of STAT3 and NF-κB activation and has the therapeutic potential for the neuroinflammation-related diseases, such as ischemic stroke.
format	article
author	Lu Yu Chu Chen Liang-Fen Wang Xi Kuang Ke Liu Hao Zhang Jun-Rong Du
author_facet	Lu Yu Chu Chen Liang-Fen Wang Xi Kuang Ke Liu Hao Zhang Jun-Rong Du
author_sort	Lu Yu
title	Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.
title_short	Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.
title_full	Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.
title_fullStr	Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.
title_full_unstemmed	Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.
title_sort	neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of nf-κb and stat3 in transient focal stroke.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/e19cbb7e890c4af0b0c008a89ea3c79a
work_keys_str_mv	AT luyu neuroprotectiveeffectofkaempferolglycosidesagainstbraininjuryandneuroinflammationbyinhibitingtheactivationofnfkbandstat3intransientfocalstroke AT chuchen neuroprotectiveeffectofkaempferolglycosidesagainstbraininjuryandneuroinflammationbyinhibitingtheactivationofnfkbandstat3intransientfocalstroke AT liangfenwang neuroprotectiveeffectofkaempferolglycosidesagainstbraininjuryandneuroinflammationbyinhibitingtheactivationofnfkbandstat3intransientfocalstroke AT xikuang neuroprotectiveeffectofkaempferolglycosidesagainstbraininjuryandneuroinflammationbyinhibitingtheactivationofnfkbandstat3intransientfocalstroke AT keliu neuroprotectiveeffectofkaempferolglycosidesagainstbraininjuryandneuroinflammationbyinhibitingtheactivationofnfkbandstat3intransientfocalstroke AT haozhang neuroprotectiveeffectofkaempferolglycosidesagainstbraininjuryandneuroinflammationbyinhibitingtheactivationofnfkbandstat3intransientfocalstroke AT junrongdu neuroprotectiveeffectofkaempferolglycosidesagainstbraininjuryandneuroinflammationbyinhibitingtheactivationofnfkbandstat3intransientfocalstroke
_version_	1718422763059806208

Neuroprotective effect of kaempferol glycosides against brain injury and neuroinflammation by inhibiting the activation of NF-κB and STAT3 in transient focal stroke.

Ejemplares similares