Literature DB >> 10927177

Cerebral ischemia: gene activation, neuronal injury, and the protective role of antioxidants.

J A Clemens1.   

Abstract

A large number of gene products appear after an ischemic insult making it difficult to decipher which genes are involved in tissue injury. Reactive oxygen species (ROS) can influence gene expression and have a role in the events that lead to neuronal death. In global cerebral ischemia the oxidative responsive transcription factor, NF-kappa B, is persistently activated in neurons that are destined to die. There are several potential routes through which NF-kappa B can act to induce neuronal death, including production of death proteins and an aborted attempt to reenter the cell cycle. NF-kappa B is only transiently activated in neurons that survive. Persistent NF-kappa B activation can be blocked by antioxidants, which suggests that the neuroprotective effect of antioxidants may be due to inhibiting activation of NF-kappa B.

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Year:  2000        PMID: 10927177     DOI: 10.1016/s0891-5849(00)00258-6

Source DB:  PubMed          Journal:  Free Radic Biol Med        ISSN: 0891-5849            Impact factor:   7.376


  21 in total

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Review 8.  Probing the molecular mechanisms of neuronal degeneration: importance of mitochondrial dysfunction and calcineurin activation.

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9.  Activation of nuclear factor kappaB in obstructive sleep apnea: a pathway leading to systemic inflammation.

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10.  Hyperlipidemia exacerbates cerebral injury through oxidative stress, inflammation and neuronal apoptosis in MCAO/reperfusion rats.

Authors:  Xiao-Lu Cao; Jing Du; Ying Zhang; Jing-Ting Yan; Xia-Min Hu
Journal:  Exp Brain Res       Date:  2015-08-04       Impact factor: 1.972

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