The Effect of NaHS on Behavioral Neurological Dysfunction Following Focal Cerebral Ischemia in Rats

Stroke is the third leading cause of death and the second cause of neurological disabilities،after alzheimer''s disease in the world. NaHS in biological systems produce hydrogen sulfide (H2S)، which will reduce damage after ischemia in different tissues. According to previous studies، NaHS protects cardiomyocytes from ischemic injury. In addition، this peptide has neuroprotective effect on mouse hippocampal and cultured cortical neurons. The present study was conducted to determine whether NaHS provides protection in transient focal cerebral ischemia.

Transient focal cerebral ischemia was induced in male Wistar rats by 60 minutes middle cerebral artery occlusion (MCAO) through using a filament method، followed by 23 hour reperfusion. Saline as a vehicle and NaHS at doses of 1، 5 and 10mg were injected intraperitoneally (IP) at the beginning of ischemia. Brain edema and motor dysfunction were assessed 24 h after MCAO.

Our results indicated that administration of NaHS at doses of 1 and 5 mg markedly reduced brain edema (P<0. 01); NaHS did not significantly change neurological dysfunction (P>0. 05).

Our present findings demonstrate that treatment with NaHS exerts its protective effects in focal cerbral ischemic models in rat.