title: Dietary supplementation with α-tocopherol reduces neuroinflammation and neuronal degeneration in the rat brain after kainic acid-induced status epilepticus.
abstract: Vitamin E (as α-tocopherol, α-T) is proposed to alleviate glia-mediated inflammation in neurological diseases, but such a role in epilepsy is still elusive. This study investigated the effect of α-T supplementation on glial activation, neuronal cell death and oxidative stress of rat brain exposed to kainate-induced seizures. Animals were fed for 2 weeks with a α-T-enriched diet (estimated intake of 750 mg/kg/day) before undergoing status epilepticus. Compliance to supplementation was demonstrated by the remarkable increase in brain α-T. Four days after seizure, brain α-T returned to baseline and lipid peroxidation markers decreased as compared to non-supplemented rats. Status epilepticus induced a lower up-regulation of astrocytic and microglial antigens (GFAP and MHC II, respectively) and production of pro-inflammatory cytokines (IL-1β and TNF-α) in supplemented than in non-supplemented animals. This anti-inflammatory effect was associated with a lower neuronal cell death. In conclusion, α-T dietary supplementation prevents oxidative stress, neuroglial over-activation and cell death occurring after kainate-induced seizures. This evidence paves the way to an anti-inflammatory and neuroprotective role of α-T interventions in epilepsy.
authors.affiliation: Department of Earth, Life and Environmental Sciences, University of Urbino Carlo Bo, I-61029 Urbino, Italy. CA126659
authors.forename: Michele
authors.initials: M
authors.lastname: Betti
authors.forename: Andrea
authors.initials: A
authors.lastname: Minelli
authors.forename: Patrizia
authors.initials: P
authors.lastname: Ambrogini
authors.forename: Stefano
authors.initials: S
authors.lastname: Ciuffoli
authors.forename: Valentina
authors.initials: V
authors.lastname: Viola
authors.forename: Francesco
authors.initials: F
authors.lastname: Galli
authors.forename: Barbara
authors.initials: B
authors.lastname: Canonico
authors.forename: Davide
authors.initials: D
authors.lastname: Lattanzi
authors.forename: Evelin
authors.initials: E
authors.lastname: Colombo
authors.forename: Piero
authors.initials: P
authors.lastname: Sestili
authors.forename: Riccardo
authors.initials: R
authors.lastname: Cuppini
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001682:Biological Availability; D001921:Brain / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D019587:Dietary Supplements; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D007608:Kainic Acid; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009410:Nerve Degeneration / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D024502:alpha-Tocopherol / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D024502:alpha-Tocopherol; D007608:Kainic Acid