丙二醛
乳酸脱氢酶
超氧化物歧化酶
海马体
一氧化氮
谷胱甘肽过氧化物酶
化学
细胞内
一氧化氮合酶
内科学
内分泌学
氧化应激
生物化学
生物
医学
酶
作者
Jing Zhao,Yang Wu,Miao Sun,Jie Wang,Yunhong Li,Kuai Zhang,Jianqiang Yu
出处
期刊:PubMed
日期:2012-01-01
卷期号:37 (1): 94-8
摘要
To investigate the protective effects of oxysophoridine (OSR) on primary cultured hippocampus neurons subjected to anoxia injury in neonatal rats and its mechanism.The model of anoxia injury of hippocampus neurons in neonatal rats were primarily cultured in vitro by physical oxygen deficiency using glucose-free culture fluid. The survival rate of neurons, the leaking rate of lactate dehydrogenase (LDH), the intracellular contents of malondialdehyde (MDA) and nitric oxide (NO), the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and nitric oxide synthase (NOS) were measured. The intracellular free calcium concentration ([Ca2+]i) in hippocampus neurons were detected with Ca(2+)-sensitive dual wavelength fluorescence spectrophotometer.Neuron death occurred in the anoxia injury model group with increase of LDH leaking rate, the contents of NO, MDA, intracellular [Ca2+] and the elevated activity of NOS while decreased activities of SOD and GSH-PX. The hippocampus neurons subjected to anoxia injury were alleviated in OSR (0.625, 5, 10 microg x L(-1)) group.OSR has significant protective effects on hippocampus neurons subjected to anoxic injury. The mechanism of its protective effect may relate to its reduction of calcium overload and against oxidation injury.
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