Different doses of dexmedetomidine reduce plasma cytokine production, brain oxidative injury, PARP and caspase expression levels but increase liver oxidative toxicity in cerebral ischemia-induced rats

AKPINAR O., NAZIROĞLU M., AKPINAR H.

BRAIN RESEARCH BULLETIN, vol.130, pp.1-9, 2017 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 130
  • Publication Date: 2017
  • Doi Number: 10.1016/j.brainresbull.2016.12.005
  • Journal Name: BRAIN RESEARCH BULLETIN
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.1-9
  • Keywords: Brain, Cerebral ischemia, Cytokine, Dexmedetomidine, Liver, Oxidative stress, N-ACETYLCYSTEINE, STRESS LEVELS, SELENIUM, REPERFUSION, VITAMIN, PLAYER, DAMAGE
  • Süleyman Demirel University Affiliated: Yes

Abstract

Cerebral ischemia-induced progression of brain, liver, and erythrocyte oxidative injuries might be modulated by dexmedetomidine (DEX) as a potent antioxidant and anti-inflammatory drug. The present study was conducted to explore whether two different doses of DEX protect against plasma cytokine and brain, liver and erythrocyte oxidative toxicity and apoptosis in cerebral ischemia-induced rats. Forty-two rats were equally divided into 7 groups. The first and second groups were used as untreated and sham controls, respectively. The third (DEX4) and fourth (DEX40) groups received 4 mg/kg and 40 mg/kg DEX treatments. The fifth, sixth and seventh group were operated on to induce cerebral ischemia. The fifth, sixth and seventh groups are used to represent cerebral ischemia, cerebral ischemia + DEX4, and cerebral ischemia + DEX40, respectively. DEX was intraperitoneally given to the DEX groups at the 3rd, 24th and 48th hour.