Kim Eun Jin, Won Ran, Sohn Jin-Hun, Chung Myung-Ae, Nam Taick Sang, Lee Hye-Jung, Lee Bae Hwan
Department of Physiology, Brain Research Institute, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, C.P.O. Box 8044, Seoul 120-752, Republic of Korea.
Biochem Biophys Res Commun. 2008 Feb 1;366(1):8-14. doi: 10.1016/j.bbrc.2007.11.050. Epub 2007 Nov 26.
Ascorbic acid (AA) and dehydroascorbic acid (DHA) have been shown to have protective effects as anti-oxidants in experimental neurological disorder models such as stroke, ischemia, and epileptic seizures. The present study was conducted to examine the protective effects of AA and DHA on kainic acid (KA) neurotoxicity using organotypic hippocampal slice cultures. After 12h KA treatment, significant delayed neuronal death was detected in the CA3, but not the CA1, region. Pretreatment with intermediate doses of AA and DHA significantly prevented cell death and inhibited reactive oxygen species (ROS) level, and mitochondrial dysfunction in the CA3 region. In contrast, pretreatment with low or high doses of AA or DHA was not effective. These data suggest that pretreatment with both AA and DHA has dose-dependent neuroprotective effects on KA-induced neuronal injury through inhibiting ROS generation and mitochondrial dysfunction.
已证明抗坏血酸（AA）和脱氢抗坏血酸（DHA）在中风、缺血和癫痫发作等实验性神经疾病模型中作为抗氧化剂具有保护作用。本研究旨在使用器官型海马切片培养物研究AA和DHA对 kainic acid（KA）神经毒性的保护作用。KA 处理 12 小时后，在 CA3 区而非 CA1 区检测到明显的延迟性神经元死亡。中等剂量的 AA 和 DHA 预处理可显著预防细胞死亡，并抑制 CA3 区的活性氧（ROS）水平和线粒体功能障碍。相比之下，低剂量或高剂量的 AA 或 DHA 预处理无效。这些数据表明，AA 和 DHA 预处理通过抑制 ROS 生成和线粒体功能障碍，对 KA 诱导的神经元损伤具有剂量依赖性神经保护作用。
