The neuroprotective effect of caffeic acid phenethyl ester on global ischemia-reperfusion injury in rat brains Rat beyinlerinde global iskemi-reperfüzyon hasarı üzerine kafeik asit fenetil esterin nöroprotektif etkisi


ALTUĞ M. E., Melek İ. M., Erdoğan S., Düzgüner V., Öztürk A., KÜÇÜKGÜL A.

Kafkas Universitesi Veteriner Fakultesi Dergisi, vol.20, no.6, pp.877-884, 2014 (SCI-Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 20 Issue: 6
  • Publication Date: 2014
  • Doi Number: 10.9775/kvfd.2014.11228
  • Journal Name: Kafkas Universitesi Veteriner Fakultesi Dergisi
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus, TR DİZİN (ULAKBİM)
  • Page Numbers: pp.877-884
  • Keywords: Antioxidant activity, Brain, cAMP-phosphodiesterase 4, CAPE, Ischemia/reperfusion, Neuroprotective effect, Rat
  • Hatay Mustafa Kemal University Affiliated: Yes

Abstract

The aim of this study was to investigate the neuroprotective effects of caffeic acid phenethyl ester (CAPE) on phosphodiesterase 4 (PDE4) mRNA isoenzymes, oxidant and antioxidant defence in ischemia/reperfusion (I/R) injured rat brains. Twenty-one rats were randomly divided into three equal groups: sham-control, ischemia/reperfusion (I/R) and I/R+CAPE. Rats in sham-control group underwent only surgical intervention without bilateral common carotid artery occlusion. Ischemia/reperfusion was induced by bilateral common carotid artery occlusion with atraumatic clips for 30 min, followed by artery reopening. The I/R+CAPE group was subjected to the same surgical procedure as I/R group, but CAPE was administered intraperitoneally at the dose of 15 μmol kg-1twice, 1 h before occlusion and at 12thh of reperfusion. The rats were sacrificed 24 h after I/R. The cAMP concentration was analyzed by ELISA and PDE4 isozyme mRNA transcriptions were evaluated by qRT-PCR methodology in the brain cortex. Ischemia-induced NO production was significantly attenuated by CAPE in the cerebral cortex. CAPE significantly enhanced GSH-Px activity, while SOD, CAT and XO activities non-significantly changed, as compared to the I/R group. CAPE significantly decreased PDE4A and PDE4B transcripts, without changing cAMP levels compared to I/R group. Ischemia-induced neurologic deficit scores were reduced by CAPE. These results suggest that CAPE slightly modulates the antioxidant defense system and NO release in rat brain during global cerebral ischemia/reperfusion injury. In addition, CAPE treatments produce the neuroprotective effect by reducing the levels of some PDE4 transcriptions.