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Ameliorating effect of quercetin on epilepsy by inhibition of inflammation in glial cells

Epilepsy is a prevalent neurological disorder and it is a significant health risk, affecting >50 million people worldwide. The development of novel and appropriate strategies is required for ameliorating the progression and/or limiting the detrimental consequences of epilepsy. In the current stud...

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Detalles Bibliográficos
Autores principales: Wu, Dongmei, Zheng, Zihui, Fan, Shaohua, Wen, Xin, Han, Xinrui, Wang, Shan, Wang, Yongjian, Zhang, Zifeng, Shan, Qun, Li, Mengqiu, Hu, Bin, Zheng, Yuanlin, Lu, Jun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7388369/
https://www.ncbi.nlm.nih.gov/pubmed/32742328
http://dx.doi.org/10.3892/etm.2020.8742
Descripción
Sumario:Epilepsy is a prevalent neurological disorder and it is a significant health risk, affecting >50 million people worldwide. The development of novel and appropriate strategies is required for ameliorating the progression and/or limiting the detrimental consequences of epilepsy. In the current study, kainic acid (KA), a neurotoxin, was used to induce seizures in mice. The flavonoid quercetin has recently been reported to have neuroprotective effects. Therefore, the effects of quercetin on KA-induced epilepsy and the potential underlying molecular mechanisms were examined. It was noted that quercetin attenuated the KA-induced seizure score and proinflammatory cytokine production, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), and activation of nuclear factor κB (NF-κB) in mice. Quercetin attenuated KA-induced proinflammatory cytokine (TNF-α and IL-1β) release from microglia cells, as well as activation of NF-κB and ionized calcium binding adapter molecule 1 in microglia cells. Therefore, quercetin inhibited KA-induced epilepsy by microglia cell inactivation and the production of NF-κB, TNF-α and IL-1β.