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硕士生靖旭论文被Toxicology and applied pharmacology(IF:4.1)接受
作者:  来源:   发布时间:2013-12-11 02:09:16  浏览次数:

Eriodictyol-7-O- glucoside activates Nrf2 and protects against

cerebral ischemic injury

 

Xu Jinga, *, Dongmei Renb, *, Xinbing Weia, Huanying Shia, Xiumei Zhanga, Ruth G. Perezc, Haiyan Loua, &, Hongxiang Loub

 

&Corresponding author:

Haiyan Lou, Ph.D, Department of Pharmacology, School of Medicine, Shandong University, No. 44 Wenhua Xi Road, Jinan, Shandong Province, 250012, PR China, Tel.: +86 531 88382605, Fax: +86 531 88383146, Email: louhaiyan@sdu.edu.cn

 

Abstract

 

Stroke is a complex disease that may involve oxidative stress-related pathways in its pathogenesis. The nuclear factor erythroid-2-related factor 2/antioxidant response element (Nrf2/ARE) pathway plays an important role in inducing phase II detoxifying enzymes and antioxidant proteins and thus has been considered a potential target for neuroprotection in stroke. The aim of the present study was to determine whether eriodictyol-7-O-glucoside (E7G), a novel Nrf2 activator, can protect against cerebral ischemic injury and to understand the role of the Nrf2/ARE pathway in neuroprotection. In primary cultured astrocytes, E7G increased the nuclear localization of Nrf2 and induced the expression of the Nrf2/ARE-dependent genes. Exposure of astrocytes to E7G provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. The protective effect of E7G was abolished by RNA interference-mediated knockdown of Nrf2 expression. In vivo administration of E7G in a rat model of focal cerebral ischemia significantly reduced the amount of brain damage and ameliorated neurological deficits. These data demonstrate that activation of Nrf2/ARE signaling by E7G is directly associated with its neuroprotection against oxidative stress-induced ischemic injury and suggest that targeting the Nrf2/ARE pathway may be a promising approach for therapeutic intervention in stroke.

 

Key words: eriodictyol-7-O-glucoside; Nrf2; astrocyte; cerebral ischemia

 

 

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