Effects of nimodipine combined with mannitol therapy on rats with cerebral ischemia reperfusion injury
Jianqing Tian
Abstract
Jianqing Tian
Abstract
Objective:To investigate the effect of nimodipine combined with mannitol therapy on rats that suffered from cerebral ischemia reperfusion injury.Method:60rats were divided randomly into3groups,treatment group and control group,each containing24rats,and12rats in normal group.Rats in treatmnet group accepted nimodipine combined with mannitol therapy after middel cerebral artery occlusion(MCAO)for one hour,while rats in control group accepted no treatment after ischemia reperfusion injury.One or three days later,rats were decapitated and their brains were extracted for SOD activity and MDA concentration assay.Immunohistochemistry was used to e鄄valuate the expression of GAP-43,MAP-2and cyclin D 1 protein.Result:SOD activity decreased in rats after is鄄chemia reperfusion injury while MDA concentration increased,compared with normal rats(P0.05).And also,level of GAP-43and MAP-2expression in rats undergone operation was lower than that of those not(P0.01),while level of cyclin D 1 expression was higher than normal(P0.01).Contrasted to control group,SOD activity in treatment group was higher and MDA concentration was lower.On the hand of immunohistochemistry,level of GAP-43and MAP-2expression in treatment group was higher than that in control group,while level of cyclin D 1 was lower.Differences between treatment group and control group were significent.Conclusion:Nimodipine combined with man鄄nitol therapy can prevent brain from ischemia reperfusion injury.Its actions of wiping free radicals out and pro鄄moting nerve regeneration are involved in the mechanism.
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Objective:To investigate the effect of nimodipine combined with mannitol therapy on rats that suffered from cerebral ischemia reperfusion injury.Method:60rats were divided randomly into3groups,treatment group and control group,each containing24rats,and12rats in normal group.Rats in treatmnet group accepted nimodipine combined with mannitol therapy after middel cerebral artery occlusion(MCAO)for one hour,while rats in control group accepted no treatment after ischemia reperfusion injury.One or three days later,rats were decapitated and their brains were extracted for SOD activity and MDA concentration assay.Immunohistochemistry was used to e鄄valuate the expression of GAP-43,MAP-2and cyclin D 1 protein.Result:SOD activity decreased in rats after is鄄chemia reperfusion injury while MDA concentration increased,compared with normal rats(P0.05).And also,level of GAP-43and MAP-2expression in rats undergone operation was lower than that of those not(P0.01),while level of cyclin D 1 expression was higher than normal(P0.01).Contrasted to control group,SOD activity in treatment group was higher and MDA concentration was lower.On the hand of immunohistochemistry,level of GAP-43and MAP-2expression in treatment group was higher than that in control group,while level of cyclin D 1 was lower.Differences between treatment group and control group were significent.Conclusion:Nimodipine combined with man鄄nitol therapy can prevent brain from ischemia reperfusion injury.Its actions of wiping free radicals out and pro鄄moting nerve regeneration are involved in the mechanism.
Key concepts: Nimodipine, Ischemia, Medicine, Reperfusion injury, Immunohistochemistry, Mannitol, Anesthesia, Occlusion