2011Journal of Tropical MedicineOpen access

Cerebral ischemic preconditioning attenuats cerebral ischemic reperfusion injury

Zhongyuan Xia

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Abstract

Objective To assess effects of cerebral ischemic preconditioning(IPC)on neuronal apoptosis and the phosphation of glycogen synthase kinase-3β(GSK-3β)after cerebral ischemic/reperfusion. Methods Thirty male Wistar rats were randomly divided into three groups:sham operation (S),ischemic/reperfusion (I/R) and ischemic preconditioning (IPC). Global brain ischemia was induced by four-VO method.Animals were killed two days after induction.Apoptosis of neurons in the cortex region were detected by TUNEL assay;infarct areas were detected by TTC;activity of p-GSK-3β was detected by spectrophotometric assay. Results Compared with the Group S, the number of TUNEL-positive cells and the infarct areas was increased in Group S and I/R(P0.01).The activity of p-GSK-3β was decreased in the I/R and IPC groups(P0.01). Compared with Group I/R,the number of TUNEL-positive cells and infarct areas was significantly decreased in group IPC (P0.01).The activity of p-GSK-3β was also increased in the group IPC(P0.01). The activity of p-GSK-3β was correlated with the increased in TUNEL-positive cells and infarct areas(P0.01). Conclusion IPC can lessen the reperfusion injury of cortex through the increase in the activity of p-GSK-3β and decrease of neuronal apoptosis.

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Objective To assess effects of cerebral ischemic preconditioning(IPC)on neuronal apoptosis and the phosphation of glycogen synthase kinase-3β(GSK-3β)after cerebral ischemic/reperfusion. Methods Thirty male Wistar rats were randomly divided into three groups:sham operation (S),ischemic/reperfusion (I/R) and ischemic preconditioning (IPC). Global brain ischemia was induced by four-VO method.Animals were killed two days after induction.Apoptosis of neurons in the cortex region were detected by TUNEL assay;infarct areas were detected by TTC;activity of p-GSK-3β was detected by spectrophotometric assay. Results Compared with the Group S, the number of TUNEL-positive cells and the infarct areas was increased in Group S and I/R(P0.01).The activity of p-GSK-3β was decreased in the I/R and IPC groups(P0.01). Compared with Group I/R,the number of TUNEL-positive cells and infarct areas was significantly decreased in group IPC (P0.01).The activity of p-GSK-3β was also increased in the group IPC(P0.01). The activity of p-GSK-3β was correlated with the increased in TUNEL-positive cells and infarct areas(P0.01). Conclusion IPC can lessen the reperfusion injury of cortex through the increase in the activity of p-GSK-3β and decrease of neuronal apoptosis.

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Available abstract

Objective To assess effects of cerebral ischemic preconditioning(IPC)on neuronal apoptosis and the phosphation of glycogen synthase kinase-3β(GSK-3β)after cerebral ischemic/reperfusion. Methods Thirty male Wistar rats were randomly divided into three groups:sham operation (S),ischemic/reperfusion (I/R) and ischemic preconditioning (IPC). Global brain ischemia was induced by four-VO method.Animals were killed two days after induction.Apoptosis of neurons in the cortex region were detected by TUNEL assay;infarct areas were detected by TTC;activity of p-GSK-3β was detected by spectrophotometric assay. Results Compared with the Group S, the number of TUNEL-positive cells and the infarct areas was increased in Group S and I/R(P0.01).The activity of p-GSK-3β was decreased in the I/R and IPC groups(P0.01). Compared with Group I/R,the number of TUNEL-positive cells and infarct areas was significantly decreased in group IPC (P0.01).The activity of p-GSK-3β was also increased in the group IPC(P0.01). The activity of p-GSK-3β was correlated with the increased in TUNEL-positive cells and infarct areas(P0.01). Conclusion IPC can lessen the reperfusion injury of cortex through the increase in the activity of p-GSK-3β and decrease of neuronal apoptosis.

Key concepts: TUNEL assay, Apoptosis, Ischemic preconditioning, Ischemia, Medicine, GSK-3, Glycogen synthase, Cerebral cortex

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