Abstract Title:

Sulforaphane is anticonvulsant and improves mitochondrial function.

Abstract Source:

J Neurochem. 2015 Sep 14. Epub 2015 Sep 14. PMID: 26365487

Abstract Author(s):

Catalina Carrasco-Pozo, Kah Ni Tan, Karin Borges

Article Affiliation:

Catalina Carrasco-Pozo


The nuclear factor erythroid 2-related factor 2 (Nrf2) pathway has been previously identified to protect the brain against various impacts. Here we investigated the effect of the Nrf2 activator sulforaphane in various seizure models and hippocampal mitochondrial bioenergetics. We found that daily injections of sulforaphane for five days elevated the seizure thresholds to 6 Hz stimulation and fluorothyl-, but not pentylenetetrazole-induced tonic seizures and protected mice against pilocarpine-induced status epilepticus (SE). Also, sulforaphane increased the antioxidant defenses within hippocampal formations and blood plasma. In addition, sulforaphane treatment reduced the extent of hippocampal lipid peroxidation 24 h post SE and protected hippocampal mitochondria against SE-induced reduction in state 2 and uncoupler-stimulated state 3 respiration. SE-mediated partial loss of rotenone-sensitive and complex II-driven respiration was reduced, consistent with the enhanced activities of complex I and II in sulforaphane-treated SE mice. In mitochondria isolated from both no SE and SE mice, sulforaphane increased state 3 respiration and respiration linked to ATP synthesis, which may contribute to its anticonvulsant and antioxidant effects by providing more ATP for cellular vital and protective functions. However, sulforaphane did not prevent SE-induced hippocampal cell death. In conclusion, sulforaphane and/or Nrf2 activation are viable anticonvulsant strategies, which are antioxidant and enhance mitochondrial function, especially the ability to produce ATP. This article is protected by copyright. All rights reserved.

Study Type : Animal Study

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