MATERIAL and METHODS: Twenty-four male Wistar albino rats were randomly divided into three groups, and administered benidipine hydrochloride (10 ?g/kg/day) orally through a catheter for 2 h to form the study group (BIR group, n=8). The I/R procedure was performed in the rats of the IR group (n=8), and a sham group was formed to determine the normal structure of the cerebral cortex (n=8). Transient ischemia was performed by clamping the left common carotid artery for 2 h. Subsequently, reperfusion was applied for 12 h. Cerebral infarct volumes were measured and cerebral cortex tissue samples were analyzed histopathologically and biochemically by measuring malondialdehyde (MDA), total glutathione, cyclooxygenase 1 (COX-1), COX-2 and superoxide dismutase (SOD)

RESULTS: The infarct area was markedly reduced in the BIR group vs. the IR group. Histopathologically, neuroprotective effects of benidipine hydrochloride were observed in the cerebral cortex tissues. The mean malondialdehyde and COX-2 levels were statistically higher in the IR group; however, in the BIR group, these levels were within the normal limits. Furthermore, the mean total glutathione, COX-1 and SOD levels were markedly lower in the IR group, and within the normal limits in the BIR group.

CONCLUSION: Benidipine hydrochloride may play a certain protective role in cerebral I/R injury. This effect may be related to improvement in the antioxidant capacity of brain tissue, and the inhibition of overproduction of inflammatory cytokines. Keywords : Cerebral ischemia reperfusion, Neuroprotection, Benidipine hydrochloride, Malondialdehyde, Glutathione, Rat