Abstract: To explore the potential impact of COX 2 on cerebral ischemic injurious mechanism,the present studies examined the influence of calcium channel blocker on the expression of COX 2,which is the key enzyme in arachidonic acid metabolism. The model of middle cerebral artery occlusion (MCAO) and immunohistochemistry staining were used to compare the expression of COX 2 protein in cerebral ischemic group with that in nimotop treatment group. There were no immunochemistry positive staining cells found among either the sham operation subgroup or the subgroup after MCAO for 1 and 4 h; however, positive staining cell began to acumulate after MCAO for 12 h. The positive cells in nimotop group were significantly higher than that in group without intervention: 12 h subgroup 56±11/mm 2 vs 45±18/mm 2(P< 0.05); 24 h subgroup 117±16/mm 2 vs 69±14/mm 2(P<0.01); 48 h subgroup 81±14/mm 2 vs 41±13/mm 2(P<0.01). The positive staining only occurred in intact neurons surrounding the core of the infarction. The infarcted area in nimotop group were significantly less than that in group of MCAO for 24 h[(28.308±3.959)mm 2 vs (46.780±6.167)mm 2, P<0,01). It indicated that Calcium channel blocker can effectively ameliorate experimental cerebral ischemic injury. The characteristics of delayed expression of COX 2 surrounding the core of infarct and the up regulation of COX 2 by calcium channel blocker, suggested that COX 2 may play a active role in the protective mechanism after ischemic cerebral injury.

Key words: cerebral ischemia, cyclooxygenase-2, calcium channel blocker