新生大鼠神经干细胞的培养方法

神经干细胞研究是目前神经科学研究的热点,如何快速经济地培养出神经干细胞是每个研究者必须面对的问题.

氯氨酮对新生大鼠缺氧缺血性脑损伤保护作用的研究

氯氨酮是一种非竞争性N甲基D天门冬氨酸(NMDA)受体拮抗剂,它能通过血脑屏障与NMDA型受体离子通道结合,阻断钙离子通道,在临床上是一种常用的诱导麻醉剂[1].竞争性或非竞争性NMDA型受体阻断剂能减轻缺氧缺血(hypoxia-ischemia, HI)所诱导的脑损伤[2].离体实验显示,氯氨酮对新生动物缺氧缺血性神经元损伤具有保护作用[3].2002年7月～2003年5月,我们对7日龄新生大鼠缺氧缺血性脑损伤(hypoxic-ischemic brain damage, HIBD)的动物模型腹腔注射氯氨酮,观察其在HIBD后的神经保护作用,报告如下.

维甲酸对新生大鼠高氧肺损伤的保护作用

胰岛素样生长因子与新生大鼠高氧肺损伤的关系

近年来的研究表明,胰岛素样生长因子(insulin-like growth factor,IGF)在肺损伤中扮演了重要角色[1].为进一步探讨其与新生儿高氧肺损伤的关系, 2002年10月～2003年6月,我们对新生大鼠高氧肺损伤模型中IGFs的表达及维甲酸(Retinoic acid,RA)干预结果进行了对比观察,现报道如下.

The electrophysiological properties of potassium ion channels are regarded as a basic index for determining the functional differentiation of neural stem cells. In this study, neural stem cells from the hippocampus of newborn rats were induced to differentiate with neurotrophic growth factor, and the electrophysiological properties of the voltage-gated potassium ion channels were observed. Immunofluorescence staining showed that the rapidly proliferating neural stem cells formed spheres in vitro that expressed high levels of nestin. The differentiated neurons were shown to express neuron-specific enolase. Flow cytometric analysis revealed that the neural stem cells were actively dividing and the percentage of cells in the S + G2/M phase was high. However, the ratio of cells in the S + G2/M phase decreased obviously as differentiation proceeded. Whole-cellpatch-clamp re-cordings revealed apparent changes in potassium ion currents as the neurons differentiated. The potassium ion currents consisted of one transient outward potassium ion current and one delayed rectifier potassium ion current, which were blocked by 4-aminopyridine and tetraethylammonium, respectively. The experimental findings indicate that neural stem cells from newborn rat hippo-campus could be cultured and induced to differentiate into functional neurons under defined condi-tions in vitro. The differentiated neurons expressed two types of outward potassium ion currents similar to those of mature neurons in vivo.

高氧肺损伤大鼠晚期糖基化终末产物受体的表达及意义

目的 探讨高氧致新生大鼠肺组织损伤过程中晚期糖基化终末产物受体(RAGE)的表达情况.方法 将16只3日龄新生大鼠依据是否高浓度氧暴露随机分为空气组(空气环境下暴露7天)大鼠和高氧组(95%氧暴露7天)大鼠,并进行比较观察.在此实验结束后,留取大鼠的肺组织标本和静脉血标本,通过光镜观察并盲法评分比较其肺组织辐射状肺泡计数(radical alveolar counts,RAC)、RT-PCR法检测肺组织匀浆RAGEmRNA表达、免疫组化法检测肺组织RAGE的表达情况、ELASA法检测血清及肺泡灌洗液(BALF)TNF及sRAGE的水平.结果 高氧组大鼠组肺组织损伤RAC降低(t=14.87,P=0.000)、肺组织RAGE mRNA增加(t=9.7109,P=0.000)、RAGE蛋白表达增加、BALF TNF-α(t=9.807,P=0.000)增高、sRAGE水平下降(t=3.7484,P=0.000).结论 RAG通路在新生大鼠高氧引致肺组织损伤中具有重要的作用.