Autophagy is upregulated in rats with status epilepticus and partly inhibited by Vitamin E

Biochem Biophys Res Commun. 2009 Feb 20;379(4):949-53. doi: 10.1016/j.bbrc.2008.12.178. Epub 2009 Jan 10.

Abstract

Autophagy, a process of bulk degradation of cellular constituents through autophagosome-lysosomal pathway, is enhanced during oxidative stress. Whether autophagy is induced during status epilepticus (SE), which induces an excess production of reactive oxygen species (ROS) and leads to oxidative stress, is not established. We also sought to determine if pretreatment with Vitamin E reduced autophagy. We used pilocarpine to elicit SE in rats. The ratio of LC3 II to LC3 I and beclin 1 were used to estimate autophagy. We found that ratio of LC3 II to LC3 I and beclin 1 increased significantly at 2, 8, 16, 24 and 72 h, peaking at 24 h after SE onset. Pretreatment with Vitamin E partially inhibited autophagy by reducing LC3 II formation and de novo synthesis of beclin 1 at 24 h after seizures. These data show that autophagy is increased in rats with pilocarpine-induced SE, and Vitamin E have a partial inhibition on autophagy.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / pharmacology*
  • Apoptosis Regulatory Proteins / biosynthesis
  • Autophagy / drug effects*
  • Beclin-1
  • Male
  • Membrane Proteins / biosynthesis
  • Microtubule-Associated Proteins / biosynthesis
  • Pilocarpine / pharmacology
  • Rats
  • Rats, Wistar
  • Status Epilepticus / chemically induced
  • Status Epilepticus / pathology*
  • Up-Regulation
  • Vitamin E / pharmacology*

Substances

  • Antioxidants
  • Apoptosis Regulatory Proteins
  • BECN1 protein, human
  • Beclin-1
  • LC3 protein, rat
  • Membrane Proteins
  • Microtubule-Associated Proteins
  • Pilocarpine
  • Vitamin E