摘要
目的 :探讨新生儿缺氧缺血脑损伤 (hypoxia ischemiabraindamage ,HIBD)后 ,脑细胞损伤的机制和黄芪对海马区的神经保护作用。方法 :用新生大鼠建立新生儿HIBD模型 ,于缺氧后不同时间点取脑 ,分别行组织病理学检查并计数海马CA1区神经细胞死亡率、免疫组化检测结扎侧海马区天冬氨酸特异酶切的半胱氨酸蛋白酶 3 (caspase 3 )蛋白的表达 ,三等分迷宫测试成熟大鼠学习记忆能力。分假手术组、模型组和黄芪治疗组观察并对比上述指标。结果 :模型组结扎侧海马caspase 3蛋白表达于缺氧缺血 (HI)后 6h轻度升高 ,2 4h达高峰 ,48h后下降 ,5d和 7d时渐恢复至基础水平。黄芪组HI后结扎侧海马神经细胞死亡率明显降低、caspase 3蛋白的表达峰值降低了 3 5 %～ 41% ,成熟大鼠的学习记忆能力明显提高。结论 :黄芪对未成熟脑HIBD后海马部位有明显的神经保护功能 ,此功能与抑制caspase 3的表达有关。
Objective To study on the mechanism of neuron death due to hypoxia-ischemia brain damage (HIBD) and the neuroprotective effects of astragulus membraneaceus on neonatal cerebral hippocampus of HIBD. Methods The neonatal hypoxia-ischemia model was established in rat pups of 7-day-old. Brain injury was examined by neuron death rate in the cerebral hippocampus CA1. Immunohistochemical staining with cysteinyl aspartate-specific proteinase (caspase-3) antibody was used to detect the changes in caspase-3 protein expression in ipsilateral hippocampus. 90 days old rats was used in tri-equal-arm maze to observe discrimination learning ability. Sham,model and astragulus membraneaceus treated groups were set up. Results In model group, caspase-3 protein showed an increase at 6、h, reaching a maximum at 24～48、h after hypoxia-ischemia. In astragulus-membraneaceus treated group, neurons death rate、caspase-3 protein were significantly reduced by astragulus membraneaceus, and discrimination learning ability of developed rats were improved obviously. Conclusion Astragulus membraneaceus produces a strong protective effect against neuronal damage in the immature rat hippocampus, along with a reduce in caspase-3 expression.
出处
《东南大学学报（医学版）》
CAS
2004年第5期291-294,共4页
Journal of Southeast University(Medical Science Edition)
基金
江苏省科委社会发展基金资助项目 (BS 980 58)
