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The aim: To see whether nimodipine had neuroprotective effects in cerebral ischemia/reperfusion injury. Materials and methods: A total of 28 adult male Sprauge-dawley rats weighting 200-300 g were distributed randomly into 4 groups (7 animals in each group): sham (neck dissection without bilateral common carotid artery occlusion), control (bilateral common carotid artery occlusion for 30 minutes and reperfusion for 1 hour), vehicle (7 days of daily carboxymethylcellulose by oral gavage followed by bilateral carotid artery occlusion and reperfusion), and nimodipine-treated rats (7 days of 3 mg/kg/day of oral Azelnidipine pretreatment then bilateral common carotid artery occlusion and reperfusion). Besides assessment of histological changes and brain infarct volume, the brain tissues were sectioned to estimate NF-κB p65, IL-6, IL-10, TNF-α, ICAM-1 and total anti-oxidant capacity. Results: Cerebral NF-κB p65, IL-6, IL-10, TNF-α, ICAM-1, in addition to cerebral infarct size were markedly increased in control and vehicle related to sham rats, while total anti-oxidant capacity was considerably decreased. Treatment with nimodipine resulted in remarkable increment of total anti-oxidant capacity, while NF-κB p65, IL-6, TNF-α, and ICAM-1 showed great reduction. Cerebral IL-10 levels didn’t change by nimodipine treatment. Histologically, control and vehicle rats showed severe brain ischemic changes which is dramatically reduced by nimodipine treatment. Conclusions: Our study results revealed that nimodipine can greatly decrease cerebral infarct size and reduce histological ischemic injury in male rats subjected to cerebral ischemia/ reperfusion. The neuroprotective actions of nimodipine possibly originated from its anti-inflammatory and antioxidative effects. Nimodipine protection was unrelated to IL-10. |
