Rosiglitazone treatment reduces hippocampal neuronal damage possibly through alleviating oxidative stress in chronic cerebral hypoperfusion

SAYAN ÖZAÇMAK H., SAYAN H., BARUT F., Jakubowska-Dogru E.

NEUROCHEMISTRY INTERNATIONAL, cilt.61, sa.3, ss.287-290, 2012 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 61 Sayı: 3
  • Basım Tarihi: 2012
  • Doi Numarası: 10.1016/j.neuint.2012.05.011
  • Dergi Adı: NEUROCHEMISTRY INTERNATIONAL
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.287-290
  • Anahtar Kelimeler: Oxidative stress, Chronic cerebral hypoperfusion, Rosiglitazone, TRANSIENT FOCAL ISCHEMIA, RECEPTOR-GAMMA AGONISTS, BRAIN, RATS, MODEL
  • Orta Doğu Teknik Üniversitesi Adresli: Evet

Özet

Oxygen free radicals and lipid peroxidation may play significant roles in the progress of injury induced by chronic cerebral hypoperfusion of the central nervous system. Rosiglitazone, a well known activator of PPAR gamma, has neuroprotective properties in various animal models of acute central nervous system damage. In the present study, we evaluate the possible impact of rosiglitazone on chronic cerebral hypoperfused-rats in regard to the levels of oxidative stress, reduced glutathione, and hippocampal neuronal damage. Chronic cerebral hypoperfusion was generated by permanent ligation of both common carotid arteries of Wistar rats for one month. Animals in treatment group were given rosiglitazone orally at doses of 1.5, 3, or 6 mg/kg per day of the 1 month duration. The treatment significantly lowered the levels of both malondialdehyde and neuronal damage, while elevated the reduced glutathione level markedly. These findings suggest that the beneficial effect of rosiglitazone on hypoperfusion-induced hippocampal neuronal damage might be the result of inhibition of oxidative insult. (c) 2012 Elsevier Ltd. All rights reserved.