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出 处:《中国急救医学》2007年第8期712-715,共4页Chinese Journal of Critical Care Medicine
基 金:国家自然科学基金资助项目(No30400483);湖南省卫生厅资助项目(NoB2005-041)
摘 要:目的探讨反复惊厥后幼鼠脑内氧化、抗氧化能力平衡的变化和神经元凋亡的关系。方法96只20日龄健康SD大鼠随机分为两组:对照组及惊厥组。通过三氟乙醚反复吸入(连续6次,每天1次)制作发育期大鼠惊厥动物模型。检测各组动物反复惊厥后6h、1d、3d、7d海马组织MDA含量、SOD活性、T-AOC水平变化,同时原位末端标记法(TUNEL)进行大鼠海马神经元凋亡检测。结果反复惊厥后6h、1d、3d海马MDA含量均较对照组显著增高,SOD活性及T-AOC水平显著降低(P<0.01),皆以第1天改变最显著,第7天三者与对照组相比较差异均无统计学意义(P>0.05);而海马神经元凋亡却于反复惊厥后1d才显著增加,持续到惊厥后7d仍显著多于对照组(P<0.01)。结论反复惊厥后海马MDA含量显著增高,SOD活性、T-AOC水平显著降低,且三者的变化皆发生在神经元凋亡增多之前,提示氧化损伤、抗氧化能力下降可能参与惊厥大鼠海马神经元凋亡的发生。Objective To investigate the changes of oxidative and antioxidative balance and their relationships with neuronal apoptosis it, the hippocampus of the developing rats following recurrent seizures. Methods 96 postnatal SD rats of 20 - day old were randomly divided into two groups : the control group and the seizure group. Seizure model of rats were induced by inhalant flurothyl daily in 6 consecutive days. Brain tissue was sampled at 6 h, 1 d, 3 d and 7 d in each group after last seizure, and the content of MDA, SOD activity and the level of T -AOC were detected; meanwhile neuronal apoptosis was also detected by TdT - mediated Dutp - biotin nick end labeling (TUNEL). Results In seizure group, the content of MDA in the hippoeampus was mnch higher than those in control group at post - seizure 6 h, 1 d, 3 d ( P 〈0. 01 ) , the activity of SOD and the level of T - AOC were obviously lower than those in control group (P 〈 0.01), and up to peak at postseizure 1 d, but there were no significant difference between the two groups at post - seizure 7 d ( P 〉 0.05 ). Neuronal apoptosis did not increase at post - seizure 6 h, but markedly increased at post - seizure 1d and lasted until 7 d ( P 〈 0.01 ). Conclusions After recurrent seizures , MDA content and neuron apoptosis increased significantly, SOD activity and T- AOC level decreased obviously. The chmlges of MDA content, SOD activity and T- AOC level were earlier than that of neuronal apoptosis. It might indicate that oxidant damage and decreasing antioxidant capacity were probably involved in the neuronal apoptosis after recurrent seizures in developing rats.
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