Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway

Xiao-Qing Jin,1,2 Fei Ye,1 Jun-Jian Zhang,1 Yan Zhao,2 Xian-Long Zhou2 1Department of Neurology, 2Emergency Center, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People’s Republic of China Abstract: Inflammation plays critical roles in the acute progression of the pathology of isc...

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Autores principales:	Jin XQ, Ye F, Zhang JJ, Zhao Y, Zhou XL
Formato:	article
Lenguaje:	EN
Publicado:	Dove Medical Press 2015
Materias:	Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/82adc5e0cee44e6cbcd9f3070531298a
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spelling	oai:doaj.org-article:82adc5e0cee44e6cbcd9f3070531298a2021-12-02T08:15:19ZTriptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway1178-2021https://doaj.org/article/82adc5e0cee44e6cbcd9f3070531298a2015-06-01T00:00:00Zhttp://www.dovepress.com/triptolide-attenuates-cerebral-ischemia-and-reperfusion-injury-in-rats-peer-reviewed-article-NDThttps://doaj.org/toc/1178-2021Xiao-Qing Jin,1,2 Fei Ye,1 Jun-Jian Zhang,1 Yan Zhao,2 Xian-Long Zhou2 1Department of Neurology, 2Emergency Center, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People’s Republic of China Abstract: Inflammation plays critical roles in the acute progression of the pathology of ischemic injury. Previous studies have shown that triptolide interferes with a number of pro-inflammatory mechanisms. In this study, we investigated whether triptolide has protective effects during acute cerebral ischemia/reperfusion (I/R) injury. Male Sprague Dawley rats received triptolide or vehicle at the onset of reperfusion following middle cerebral artery occlusion. Twenty-four hours after reperfusion, we evaluated neurological injuries, the expression of pro-inflammatory markers, and NF-κB activation. I/R rats treated with triptolide showed significantly better neurological deficit scores, decreased neural apoptosis, and reduced cerebral infarct volume and brain edema, and triptolide treatment suppressed the activation of NF-κB following I/R injury. Furthermore, the expression levels of pro-inflammatory cytokines at both the mRNA and protein levels were significantly decreased in rats receiving triptolide. These results indicate that the neuroprotective effects of triptolide during acute cerebral I/R injury are possibly related to the inhibition of both the NF-κB signaling pathway and inflammation. Keywords: ischemic stroke, inflammation, rat model, NF-κB pathwayJin XQYe FZhang JJZhao YZhou XLDove Medical PressarticleNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol 2015, Iss default, Pp 1395-1403 (2015)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429
spellingShingle	Neurosciences. Biological psychiatry. Neuropsychiatry RC321-571 Neurology. Diseases of the nervous system RC346-429 Jin XQ Ye F Zhang JJ Zhao Y Zhou XL Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway
description	Xiao-Qing Jin,1,2 Fei Ye,1 Jun-Jian Zhang,1 Yan Zhao,2 Xian-Long Zhou2 1Department of Neurology, 2Emergency Center, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, People’s Republic of China Abstract: Inflammation plays critical roles in the acute progression of the pathology of ischemic injury. Previous studies have shown that triptolide interferes with a number of pro-inflammatory mechanisms. In this study, we investigated whether triptolide has protective effects during acute cerebral ischemia/reperfusion (I/R) injury. Male Sprague Dawley rats received triptolide or vehicle at the onset of reperfusion following middle cerebral artery occlusion. Twenty-four hours after reperfusion, we evaluated neurological injuries, the expression of pro-inflammatory markers, and NF-κB activation. I/R rats treated with triptolide showed significantly better neurological deficit scores, decreased neural apoptosis, and reduced cerebral infarct volume and brain edema, and triptolide treatment suppressed the activation of NF-κB following I/R injury. Furthermore, the expression levels of pro-inflammatory cytokines at both the mRNA and protein levels were significantly decreased in rats receiving triptolide. These results indicate that the neuroprotective effects of triptolide during acute cerebral I/R injury are possibly related to the inhibition of both the NF-κB signaling pathway and inflammation. Keywords: ischemic stroke, inflammation, rat model, NF-κB pathway
format	article
author	Jin XQ Ye F Zhang JJ Zhao Y Zhou XL
author_facet	Jin XQ Ye F Zhang JJ Zhao Y Zhou XL
author_sort	Jin XQ
title	Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway
title_short	Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway
title_full	Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway
title_fullStr	Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway
title_full_unstemmed	Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway
title_sort	triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa b signaling pathway
publisher	Dove Medical Press
publishDate	2015
url	https://doaj.org/article/82adc5e0cee44e6cbcd9f3070531298a
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Triptolide attenuates cerebral ischemia and reperfusion injury in rats through the inhibition the nuclear factor kappa B signaling pathway

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