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宫内缺血缺氧致胚鼠脑细胞损伤凋亡的实验研究 被引量:2

Pathological Changes and Apoptosis of Brain Cells in Rat Embryo Saffering from Intrauterine Hypoxia-ischemic Injury
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摘要 目的 采用胚鼠宫内窘迫的动物模型 ,观察胚鼠缺血缺氧性脑损伤后不同时间点脑细胞的病理变化及损伤凋亡的情况。方法 孕 17d(孕中期 )孕鼠 ,实验组钳夹子宫动脉 30 m in后 ,恢复血供。缺血后 2 4 h、4 8h及72 h取标本。对照组行同期开关腹术 ,但不钳夹子宫动脉。与实验组对应的相同时间取标本。用 HE,尼氏染色 ,胆碱酯酶染色 ,TU NEL及电镜在镜下观察脑组织的病理改变。结果 胚鼠缺血缺氧 30 min,脑组织可见出血 ,神经细胞发生水肿、变性 ;尼氏体形态变化 ,溶解 ;胆碱酯酶活性减弱 ;缺血再灌注后 2 4 h即出现凋亡细胞 ,并随缺血再灌注时间的延长逐渐增多。结论 宫内窘迫所致胚鼠缺血缺氧可造成神经细胞的严重损伤和凋亡。 Objective To observe the pathological changes of fetal rat brain cells caused by transient intrauterine ischemia in pregnant rats. Methods The uterine arteries of the pregnant rats at 17 days of gestation were clamped for 30 min in the experimental group, the samples were collected 24, 48 and 72 hours respectively after the clamping of artery, respectivly. In control group, the pregnent rat's abdomens were cut open and closed but the uterine arteries were kept intact; the samples were collected 24, 48 and 72 hours after the sham openration, respectively. The pathological changes of brain tissues were observed under light microscope by HE, Nissl, cholinesterase staining, sequential TUNEL technique, and by electron microscopy as well. Results The edema, degeneration of neural cells and the hemorrhage of brain were observed in experimental group. The Nissl bodies and the activity of cholinesterase decreased. The apoptosis cells appeared 24 hours after hypoxia-ischemia injury and increased progressively with time. Conclusion Uterine hypoxia and ischemia can cause severe damage to neural cells of fetal rat.
出处 《四川大学学报(医学版)》 CAS CSCD 北大核心 2004年第3期354-357,共4页 Journal of Sichuan University(Medical Sciences)
基金 教育部博士点基金 (批准号 2 0 0 2 0 610 0 2 8)资助
关键词 胚鼠 宫内窘迫 凋亡 Embryo Intrauterine hypoxia Apoptosis
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