Ephedrine protects hippocampal neurons in neonatal rats after hypoxic-ischemic brain injury
Xiaoping Zhang
Abstract
Xiaoping Zhang
Abstract
Objective To explore the effects of ephedrine on the hippocampal cell apoptosis and behavioral performance after hypoxia-ischemia brain injury in neonatal rats.Methods Totally 90 7-day rats were randomly divided into 3 groups,ephedrine treatment group,model group,and sham group.Hypoxia-ischemia brain injury model was established by permanently ligating right common carotid artery.Ephedrine (1.5 mg/kg,once per day) was injected intraperitoneally to the rats of ephedrine treatment group for 7 d,and the rats of model group was given normal saline at the same volume.At the following time interval of 6 and 12 h,and 1,3,and 7 d after hypoxia,the expression of bcl-2 and bax were detected in the hippocampal region by immunohistochemical staining.At 4 weeks after surgery,behavioral changes in the remaining rats were tested by Morris water maze.Results Compared with model group,the expression of bcl-2 in the ephedrine treatment group was significantly increased after hypoxic-ischemic injury,peaked at 1 d and decreased in 3 d after operation.And the expression of bax in the ephedrine treatment group was decreased in 1 d after hypoxic-ischemia.The average time of escape latency was gradually decreased in each group.However,from the 3rd to 5th day,it was much shorter in ephedrine treatment group than in model group.In addition,the frequency platform passing in the ephedrine treatment group and the percentage of swimming distance traveled in the previous target quadrant was significantly greater than those of the control group.Conclusion Ephedrine upregulates bcl-2 and downregulates bax in the hippocampus of neonatal rats after hypoxia-ischemia,and improves their ability of learning and memory.
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Objective To explore the effects of ephedrine on the hippocampal cell apoptosis and behavioral performance after hypoxia-ischemia brain injury in neonatal rats.Methods Totally 90 7-day rats were randomly divided into 3 groups,ephedrine treatment group,model group,and sham group.Hypoxia-ischemia brain injury model was established by permanently ligating right common carotid artery.Ephedrine (1.5 mg/kg,once per day) was injected intraperitoneally to the rats of ephedrine treatment group for 7 d,and the rats of model group was given normal saline at the same volume.At the following time interval of 6 and 12 h,and 1,3,and 7 d after hypoxia,the expression of bcl-2 and bax were detected in the hippocampal region by immunohistochemical staining.At 4 weeks after surgery,behavioral changes in the remaining rats were tested by Morris water maze.Results Compared with model group,the expression of bcl-2 in the ephedrine treatment group was significantly increased after hypoxic-ischemic injury,peaked at 1 d and decreased in 3 d after operation.And the expression of bax in the ephedrine treatment group was decreased in 1 d after hypoxic-ischemia.The average time of escape latency was gradually decreased in each group.However,from the 3rd to 5th day,it was much shorter in ephedrine treatment group than in model group.In addition,the frequency platform passing in the ephedrine treatment group and the percentage of swimming distance traveled in the previous target quadrant was significantly greater than those of the control group.Conclusion Ephedrine upregulates bcl-2 and downregulates bax in the hippocampus of neonatal rats after hypoxia-ischemia,and improves their ability of learning and memory.
Key concepts: Ephedrine, Hippocampal formation, Medicine, Anesthesia, Morris water navigation task, Ischemia, Hypoxia (environmental), Saline