Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Activation of Nrf2-ARE signal pathway protects the brain from damage induced by epileptic seizure.

Authors: Wang, W  Wu, Y  Zhang, G  Fang, H  Wang, H  Zang, H  Xie, T  Wang, W 
Citation: Wang W, etal., Brain Res. 2014 Jan 28;1544:54-61. doi: 10.1016/j.brainres.2013.12.004. Epub 2013 Dec 10.
Pubmed: (View Article at PubMed) PMID:24333359
DOI: Full-text: DOI:10.1016/j.brainres.2013.12.004

Epilepsy remains a major medical problem for which there is no effective treatment. Oxidative damage plays an important role in epilepsy pathogenesis and may represent a target for treatment of epilepsy. Recent studies have suggested that nuclear factor erythroid 2-related factor 2 (Nrf2) binds to antioxidant response element (ARE) to induce antioxidant and phase II detoxification enzymes under conditions of oxidative stress, which reduces oxidative damage and accumulation of toxic metabolites. This study evaluated the role of Nrf2-ARE signal pathway in protecting the brain from seizure-mediated damage. Wistar rats and Nrf2-deficient or control mice were chronic kindled in the amygdala. Sulforaphane (SF) was used to activate Nrf2-ARE signal pathway. The progression of kindling, the cognitive impairment and oxidative stress parameters were assessed to determine the extent of seizure-mediated brain damage. Our results indicate that activation Nrf2-ARE signal pathway with SF in hippocampus suppressed the progression of amygdala kindling, and also ameliorated the cognitive impairment and oxidative stress induced by epileptic seizure. These observations suggest that Nrf2-ARE signal pathway may represent a strategic target for epilepsy therapies.

Annotation

Disease Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 10412723
Created: 2015-11-23
Species: All species
Last Modified: 2015-11-23
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.