Protection of propofol on cerebral ischemia reperfusion injury in rats and its mechanism of intervention for Caspase-3
Qiao Li
Abstract
Qiao Li
Abstract
Objective To observe the effects of propofol ip injection on hippocampus nervous after cerebral ischemia-reperfusion injury, to study the prevention of propofol to cerebral ischemia-reperfusion injury during clinical peroperative period. Methods Sixty SD rats were randomly divided into propofol group, Sham group, and model group. Left cerebral arterial embolism models were made. At 10 min before cerebral ischemia-reperfusion, rats in propofol group were ip administered propofol(50 mg/kg), and physiological saline was given to Sham group. Rats in model group were done the same operation except cerebral ischemia-reperfusion and propofol. At 24 h after ischemia reperfusion, the tissues were collected. The areas of left cerebral infarct of rats were measured by TTC staining method, Caspase-3 express in hippocampus was measured by immunohistochemical methods, and transcriptional levels of Caspase-3 m RNA were detected by in situ hybridization test. Results Compared with model group, gray area obviously shrank and incanus areas were improved in propofol group. The expression of Caspase-3 and transcriptional levels of Caspase-3 m RNA in hippocampus of rats in propofol group were lower than those in model group, with significant differences between two groups(P 0.01). Conclusion Propofol intervention before ischemia-reperfusion maybe prevent ischemia reperfusion injury, and the mechanism is related to the apoptosis signal transduction pathway through Caspase-3 mediation.
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Objective To observe the effects of propofol ip injection on hippocampus nervous after cerebral ischemia-reperfusion injury, to study the prevention of propofol to cerebral ischemia-reperfusion injury during clinical peroperative period. Methods Sixty SD rats were randomly divided into propofol group, Sham group, and model group. Left cerebral arterial embolism models were made. At 10 min before cerebral ischemia-reperfusion, rats in propofol group were ip administered propofol(50 mg/kg), and physiological saline was given to Sham group. Rats in model group were done the same operation except cerebral ischemia-reperfusion and propofol. At 24 h after ischemia reperfusion, the tissues were collected. The areas of left cerebral infarct of rats were measured by TTC staining method, Caspase-3 express in hippocampus was measured by immunohistochemical methods, and transcriptional levels of Caspase-3 m RNA were detected by in situ hybridization test. Results Compared with model group, gray area obviously shrank and incanus areas were improved in propofol group. The expression of Caspase-3 and transcriptional levels of Caspase-3 m RNA in hippocampus of rats in propofol group were lower than those in model group, with significant differences between two groups(P 0.01). Conclusion Propofol intervention before ischemia-reperfusion maybe prevent ischemia reperfusion injury, and the mechanism is related to the apoptosis signal transduction pathway through Caspase-3 mediation.
Key concepts: Propofol, Ischemia, Medicine, Reperfusion injury, Anesthesia, Apoptosis, Pharmacology, Internal medicine