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: | , , , , |
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| Formato: | article |
| Lenguaje: | EN |
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Dove Medical Press
2015
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/82adc5e0cee44e6cbcd9f3070531298a |
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| Sumario: | 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 |
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