2009Int J Cerebrovasc DisRequires access

Expression of extracellular signal-regulated kinase 1/2 and neuronal apoptosis in hippocampal CA4 region after cerebral ischemia-reperfusion in diabetic rats

Yi Ma, Jing Li, Fengying Guo

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Abstract

Objective To investigate the expression of neuronal extracellular signalregulated kinase 1/2 (ERK1/2) and its significance after cerebral ischemia reperfusion in diabetic rats. Methods Seventy-two healthy adult SD rats were randomly divided into shamoperation, normal glucose with cerebral ischemia and diabetes with cerebral ischemia groups. Each group was redivided into ischemia 15 minutes and reperfusion 1, 3 and 6 h subgroups according to the different time points of ischemia reperfusion (n = 6 in each subgroup). Streptozocin was used to induce diabetes, and a global cerebral ischemia model of diabetic rat was established by the bilateral vascular occlusion combining with bloodletting. TUNEL and immunohistochemistry were used to observe neuronal apoptosis and the expression of the phosphorylation of ERK1/2 in hippocampal CA4 region. Results The incidences of neuronal apoptosis in hippocampal CA4 region for ischemia 15 minutes and reperfusion 1,3 and 6 h in the diabetes with cerebral ischemia group were significantly higher than those in the normal glucose with cerebral ischemia group (P 〈 0.05); the expressions of the phosphorylation of ERK1/2 at all time points in the diabetes with cerebral ischemia group were higher, and reperfusion 1 and 3 h were significantly higher than those in the normal glucose with cerebral ischemia group (P 〈 0.01 ). Conclusions ERK1/2 might involved in the mechanism of neuronal injury after diabetes aggravating cerebral ischemia-reperfusion. Key words: diabetes mellitus;  cerebral ischemia;  reperfusion injury;  mitogen-activated protein kinase 1 ;  apoptosis;  rats

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Objective To investigate the expression of neuronal extracellular signalregulated kinase 1/2 (ERK1/2) and its significance after cerebral ischemia reperfusion in diabetic rats. Methods Seventy-two healthy adult SD rats were randomly divided into shamoperation, normal glucose with cerebral ischemia and diabetes with cerebral ischemia groups. Each group was redivided into ischemia 15 minutes and reperfusion 1, 3 and 6 h subgroups according to the different time points of ischemia reperfusion (n = 6 in each subgroup). Streptozocin was used to induce diabetes, and a global cerebral ischemia model of diabetic rat was established by the bilateral vascular occlusion combining with bloodletting. TUNEL and immunohistochemistry were used to observe neuronal apoptosis and the expression of the phosphorylation of ERK1/2 in hippocampal CA4 region. Results The incidences of neuronal apoptosis in hippocampal CA4 region for ischemia 15 minutes and reperfusion 1,3 and 6 h in the diabetes with cerebral ischemia group were significantly higher than those in the normal glucose with cerebral ischemia group (P 〈 0.05); the expressions of the phosphorylation of ERK1/2 at all time points in the diabetes with cerebral ischemia group were higher, and reperfusion 1 and 3 h were significantly higher than those in the normal glucose with cerebral ischemia group (P 〈 0.01 ). Conclusions ERK1/2 might involved in the mechanism of neuronal injury after diabetes aggravating cerebral ischemia-reperfusion. Key words: diabetes mellitus;  cerebral ischemia;  reperfusion injury;  mitogen-activated protein kinase 1 ;  apoptosis;  rats

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Available abstract

Objective To investigate the expression of neuronal extracellular signalregulated kinase 1/2 (ERK1/2) and its significance after cerebral ischemia reperfusion in diabetic rats. Methods Seventy-two healthy adult SD rats were randomly divided into shamoperation, normal glucose with cerebral ischemia and diabetes with cerebral ischemia groups. Each group was redivided into ischemia 15 minutes and reperfusion 1, 3 and 6 h subgroups according to the different time points of ischemia reperfusion (n = 6 in each subgroup). Streptozocin was used to induce diabetes, and a global cerebral ischemia model of diabetic rat was established by the bilateral vascular occlusion combining with bloodletting. TUNEL and immunohistochemistry were used to observe neuronal apoptosis and the expression of the phosphorylation of ERK1/2 in hippocampal CA4 region. Results The incidences of neuronal apoptosis in hippocampal CA4 region for ischemia 15 minutes and reperfusion 1,3 and 6 h in the diabetes with cerebral ischemia group were significantly higher than those in the normal glucose with cerebral ischemia group (P 〈 0.05); the expressions of the phosphorylation of ERK1/2 at all time points in the diabetes with cerebral ischemia group were higher, and reperfusion 1 and 3 h were significantly higher than those in the normal glucose with cerebral ischemia group (P 〈 0.01 ). Conclusions ERK1/2 might involved in the mechanism of neuronal injury after diabetes aggravating cerebral ischemia-reperfusion. Key words: diabetes mellitus;  cerebral ischemia;  reperfusion injury;  mitogen-activated protein kinase 1 ;  apoptosis;  rats

Key concepts: Ischemia, Medicine, Diabetes mellitus, TUNEL assay, Internal medicine, Endocrinology, Apoptosis, Anesthesia

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Expression of extracellular signal-regulated kinase 1/2 and neuronal apoptosis in hippocampal CA4 region after cerebral ischemia-reperfusion in diabetic rats — Research Paper | ScholarLens