This study was performed to evaluate the neuroprotective effect of Azelnidipine in cerebral ischemia/reperfusion and to envisage its mechanisms. Twenty-eight adult male Sprague-Dawley rats weighing 200–300 g were randomized into 4 groups (7 rats in each group). Sham (neck dissection without bilateral common carotid artery occlusion), control (30 minutes of bilateral common carotid artery occlusion and reperfusion for 1 hour), vehicle (identical volume of 0.3% carboxymethylcellulose (CMC) orally every day then bilateral common artery occlusion and reperfusion), and Azelnipine-treated rats (7 days of Azelnidipine pretreatment 3 mg/kg/day followed by bilateral common carotid artery occlusion and reperfusion). In addition to brain infarct volume and histopathological assessment, the brain tissues were harvested to evaluate cerebral IL-6, IL-10, TNF-α, ICAM-1, NF-κB p65, and total antioxidant capacity levels. Cerebral levels of IL-6, IL-10, TNF-α, NF-κB p65, and ICAM-1, besides cerebral infarct volume, were significantly elevated in control and vehicle related to sham groups, while total antioxidant capacity was markedly reduced. Azelnidipine treatment resulted in remarkable upregulation of total antioxidant capacity; meanwhile, IL-6, TNF-α, NF-κB p65, and ICAM-1 showed a considerable reduction. Cerebral IL-10 levels were not affected by Azelnidipine pretreatment. Histologically, control and vehicle rats showed severe ischemic injury, which was greatly reversed by Azelnidipine treatment. The current study disclosed that Azelnidipine could markedly reduce cerebral infarct volume and ameliorate histopathological damage in male rats exposed to cerebral ischemia/reperfusion. The neuroprotective effects of Azelnidipine probably stemmed from its anti-inflammatory and antioxidative properties. Azelnidipine had no effect on cerebral IL-10 levels.

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.