摘要
目的研究缺氧再灌对皮层神经元的影响以及氯胺酮和右美沙芬的保护作用。方法采用１６～１８ｄ胎龄的大鼠皮层细胞分离培养，以培养上清液中乳酸脱氢酶（ＬＤＨ）活性作为细胞损伤的指标。结果培养１２ｄ的细胞先置于缺氧环境中５ｈ，再灌０～２４ｈ后，随着缺氧再灌时间延长，ＬＤＨ漏出增加。缺氧再灌前，于培养液中加入氯胺酮或右美沙芬，则ＬＤＨ漏出量均明显低于对照组。结论缺氧和再灌均造成皮层神经元严重损伤，氯胺酮和右美沙芬对上述损伤有明显的保护作用；说明ＮＭＤＡ（Ｎ－ｍｅｔｈｙｌ－Ｄ－ａｓｐａｒｔａｔｅ）受体在缺血性脑损伤过程起着至关重要的作用。
Objective: To examine the effects of anoxia/reoxygenation (A/R) on cultured cortical neurons and the protective effects of ketamine and dextromethorphan. Methods: The cortical neurons were from 16 to 18-day-old fetal rats,and the cell damage was assessed by lactate dehydrogenase (LDH) release into culture medium. Results: The cultrues of 12 days were exposed to anoxia (5h) followed by reoxygenation (0～24h). As the A/R proceeded, the release of LDH into the bathing medium increased obviously. When the cultures were pretreated with ketamine or dextromethorphan before A/R, the values of LDH efflux in culture medium were significantly lower than those of controls. Conclutions: The cultured cortical neurons are seriously damaged by A/R. Such damages could be attenuated by ketamine and dextromethorphan, suggesting that NMDA (N-methyl-D-aspartate) receptors play an important role in the process of ischemia-induced damage in the brain.
出处
《徐州医学院学报》
CAS
1996年第4期337-339,共3页
Acta Academiae Medicinae Xuzhou
基金
国家自然科学基金
关键词
氯胺酮
右美沙芬
神经元
缺氧
细胞培养
ketamine
dextromethorphan
anoxia/reoxygenation
cortical neuron
cell culture
