Activation of peroxisome proliferator-activated receptor β/δ attenuates acute ischemic stroke on middle cerebral ischemia occlusion in rats

J Stroke Cerebrovasc Dis. 2014 Jul;23(6):1396-402. doi: 10.1016/j.jstrokecerebrovasdis.2013.11.021. Epub 2014 Apr 26.

Abstract

Background: Peroxisome proliferator-activated receptor (PPAR)-β/δ is a transcription factor that belongs to the nuclear hormone receptor family. There is little information about the effects of the immediate administration of specific ligands of PPAR-β/δ (GW0742) in animal models of acute ischemic stroke. Using a rat model of middle cerebral ischemia occlusion (MCAO) in vivo, we have investigated the effect of pretreatment with GW0742 before MCAO.

Methods: The neuroprotective effect of GW0742 against acute ischemic stroke was evaluated by the neurologic deficit score (NDS), dry-wet weight, and 2,3,5-triphenyltetrazolium chloride staining. The levels of interleukin (IL)-1β, nuclear factor (NF)-κB, and tumor necrosis factor (TNF)-α were detected by an enzyme-linked immunosorbent assay. The expressions of inducible nitric oxide synthase (iNOS), Bax, and Bcl-2 were detected by Western blot. The apoptotic cells were counted by in situ terminal deoxyribonucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling assay.

Results: The pretreatment with GW0742 significantly increased the expression of Bcl-2, and significantly decreased in the volume of infarction, NDS, edema, expressions of IL-1β, NF-κB, TNFα, and Bax, contents of iNOS and the apoptotic cells in infarct cerebral hemisphere compared with rats in the vehicle group at 24 hours after MCAO.

Conclusions: The study suggests the neuroprotective effect of the PPAR-β/δ ligand GW0742 in acute ischemic stroke by a mechanism that may involve its anti-inflammatory and antiapoptotic action.

Keywords: GW0742; PPAR-β/δ; anti-inflammatory; middle cerebral artery occlusion (MCAO); rat.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Brain / drug effects
  • Brain / pathology
  • Brain / physiopathology
  • Brain Ischemia / drug therapy*
  • Brain Ischemia / pathology
  • Brain Ischemia / physiopathology
  • Infarction, Middle Cerebral Artery / drug therapy*
  • Infarction, Middle Cerebral Artery / pathology
  • Infarction, Middle Cerebral Artery / physiopathology
  • Interleukin-1beta / metabolism
  • Male
  • Motor Activity / drug effects
  • Motor Activity / physiology
  • NF-kappa B / metabolism
  • PPAR delta / agonists*
  • PPAR-beta / agonists*
  • Rats
  • Rats, Sprague-Dawley
  • Stroke / drug therapy*
  • Stroke / physiopathology
  • Thiazoles / pharmacology
  • Thiazoles / therapeutic use*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Interleukin-1beta
  • NF-kappa B
  • PPAR delta
  • PPAR-beta
  • Thiazoles
  • Tumor Necrosis Factor-alpha
  • (4-(((2-(3-fluoro-4-(trifluoromethyl)phenyl)-4-methyl-1,3-thiazol-5-yl)methyl)sulfanyl)-2-methylphenoxy)acetic acid