2012•The Journal of Clinical AnesthesiologyRequires access

Effect of ketamine on apoptosis and TNF-β,IL-10 of hippocampal cells in global cerebral ischemic reperfusion injury rabbits

Chen Qian-fe

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Abstract

Objective To explore the effect of ketamine on apoptosis and the expression of tumor necrosis factor(TNF)-β, interleukin(IL)-10 of hippocampal cells in global cerebral ischemic reperfusion injury rabbits. Methods Forty-five adult healthy New Zealand white rabbits were equally randomized into three groups (n=15): sham operation group (group A), model group (group B) and model + ketamine group (group C). The model of global cerebral ischemia-reperfusion was produced by femoral arterial bloodletting combined common carotid occlusion (30 min). Ketamine 4.5 mg/kg was injected through femoral vein after carotid occlusion in group C. The survived neurons in the CA1 region of the hippocampus were observed by HE staining, and apoptosis was detected by TUNEL method. The numbers of TNF-β and IL-10 positive neurons were detected by immunohistochemical stains. Results Compared with group B, the number of survival cells increased significantly in group C after 12-72 h of reperfusion (P0.05); the number of apoptosis cells decreased significantly in group C after 12-72 h of reperfusion (P0.01). The positive expressions of TNF-β were higher in group B and C than in group A after 6-72 h of reperfusion(P0.05), while the positive expressions of TNF-β were lower in group C than in group B after 6 h and 72 h of reperfusion(P0.05). After 6 h of reperfusion, the positive expressions of IL-10 were higher in group C than in group A and B(P0.05), while IL-10 were lower in group C after 72 h of reperfusion(P0.05). Conclusion Ketamine protects brain injury through reducing inflammatory responses and decreasing the necrosis and apoptosis after global cerebral ischem ia-reperfusion in rabbits.

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Objective To explore the effect of ketamine on apoptosis and the expression of tumor necrosis factor(TNF)-β, interleukin(IL)-10 of hippocampal cells in global cerebral ischemic reperfusion injury rabbits. Methods Forty-five adult healthy New Zealand white rabbits were equally randomized into three groups (n=15): sham operation group (group A), model group (group B) and model + ketamine group (group C). The model of global cerebral ischemia-reperfusion was produced by femoral arterial bloodletting combined common carotid occlusion (30 min). Ketamine 4.5 mg/kg was injected through femoral vein after carotid occlusion in group C. The survived neurons in the CA1 region of the hippocampus were observed by HE staining, and apoptosis was detected by TUNEL method. The numbers of TNF-β and IL-10 positive neurons were detected by immunohistochemical stains. Results Compared with group B, the number of survival cells increased significantly in group C after 12-72 h of reperfusion (P0.05); the number of apoptosis cells decreased significantly in group C after 12-72 h of reperfusion (P0.01). The positive expressions of TNF-β were higher in group B and C than in group A after 6-72 h of reperfusion(P0.05), while the positive expressions of TNF-β were lower in group C than in group B after 6 h and 72 h of reperfusion(P0.05). After 6 h of reperfusion, the positive expressions of IL-10 were higher in group C than in group A and B(P0.05), while IL-10 were lower in group C after 72 h of reperfusion(P0.05). Conclusion Ketamine protects brain injury through reducing inflammatory responses and decreasing the necrosis and apoptosis after global cerebral ischem ia-reperfusion in rabbits.

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Available abstract

Objective To explore the effect of ketamine on apoptosis and the expression of tumor necrosis factor(TNF)-β, interleukin(IL)-10 of hippocampal cells in global cerebral ischemic reperfusion injury rabbits. Methods Forty-five adult healthy New Zealand white rabbits were equally randomized into three groups (n=15): sham operation group (group A), model group (group B) and model + ketamine group (group C). The model of global cerebral ischemia-reperfusion was produced by femoral arterial bloodletting combined common carotid occlusion (30 min). Ketamine 4.5 mg/kg was injected through femoral vein after carotid occlusion in group C. The survived neurons in the CA1 region of the hippocampus were observed by HE staining, and apoptosis was detected by TUNEL method. The numbers of TNF-β and IL-10 positive neurons were detected by immunohistochemical stains. Results Compared with group B, the number of survival cells increased significantly in group C after 12-72 h of reperfusion (P0.05); the number of apoptosis cells decreased significantly in group C after 12-72 h of reperfusion (P0.01). The positive expressions of TNF-β were higher in group B and C than in group A after 6-72 h of reperfusion(P0.05), while the positive expressions of TNF-β were lower in group C than in group B after 6 h and 72 h of reperfusion(P0.05). After 6 h of reperfusion, the positive expressions of IL-10 were higher in group C than in group A and B(P0.05), while IL-10 were lower in group C after 72 h of reperfusion(P0.05). Conclusion Ketamine protects brain injury through reducing inflammatory responses and decreasing the necrosis and apoptosis after global cerebral ischem ia-reperfusion in rabbits.

Key concepts: Medicine, Apoptosis, Reperfusion injury, Group A, TUNEL assay, Anesthesia, Ketamine, Hippocampal formation

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