Investigation of neuroprotective effect of dexamethasone by using nitric oxide and leukocyte levels in experimental head trauma


Demir O., KIYMAZ N., Ekin S. , YILMAZ N., OZBEK H.

INTERNATIONAL JOURNAL OF NEUROSCIENCE, cilt.117, ss.1719-1730, 2007 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 117 Konu: 12
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1080/00207450500514284
  • Dergi Adı: INTERNATIONAL JOURNAL OF NEUROSCIENCE
  • Sayfa Sayıları: ss.1719-1730

Özet

The objective of the present study was to determine the levels of nitric oxide (NO) and white blood cells (WBCs), which are assumed to play a role in secondary cerebral damage by increasing to pathological levels during cranial trauma, and to investigate the neuroprotective effect of dexamethasone on NO and WBC levels in experimental cranial trauma. For this purpose, adult Sprague-Dawley male rats were used. Blood NO and WBC levels were investigated in one group of non-trauma rats (control group, n = 10) after 6 h; in a group of rats with experimental post-cranial trauma (trauma group, n = 10) after 6 and 24 h; and in a third group of rats with experimental cranial trauma, intraperitoneally injected with 10 mg/kg dexamethasone after 1 and 12 h (trauma + dexamethasone group, n = 10), WBC and NO levels were measured after 6 and 24 h. Determination of NO levels was carried out by assaying serum nitrite and nitrate levels. The increases in post-trauma serum NO (nitrite and nitrate) and WBC levels were statistically significant for the trauma and trauma + dexamethasone groups compared to controls. There was no significant difference between serum NO and WBC levels in rats in the trauma + dexamethasone and those in the trauma group. The study demonstrated no significant inhibition of NO and WBC levels by dexamethasone, a drug used for its anti-edema and anti-inflammatory effects and its influence on membrane stabilization and in avoiding oscillation stress. In the present study, dexamethasone was found to be ineffective in decreasing NO and WBC levels to avoid secondary cerebral damage after cranial trauma.