Effects of acetylpuerarin on hippocampal neurons and intracellular free calcium subjected to oxygen–glucose deprivation/reperfusion in primary culture
Effects of acetylpuerarin on hippocampal neurons and intracellular free calcium subjected to oxygen–glucose deprivation/reperfusion in primary culture
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乙酰葛根素对原代培养物氧糖剥夺/再灌注海马神经元和细胞内游离钙的影响
DOI：
10.1016/j.brainres.2007.01.146
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发表时间：
2007
期刊：
影响因子：
2.9
通讯作者：
Xiu
中科院分区：
文献类型：
--
作者：
R. Liu;Xin Wei;Xiu
目的探讨乙酰葛根素对氧糖剥夺/再灌注原代培养物海马神经元和细胞内游离钙的影响。方法根据不同再灌注时间（1 h、6 h、12 h、24 h），采用3种浓度（1.6 μmol l−1、0.4 μmol l−1、0.1 μmol l−1）的乙酰葛根素，阳性对照药物MK-801（10 μmol l−1），将神经元随机分为21组。倒置相差显微镜观察各组；通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物 (MTT) 的还原来测量神经元活力；采用Fura-2/AM酯荧光分光光度计观察细胞内Ca2+。结果乙酰葛根素和MK-801治疗组损伤的神经元受到保护，变性坏死减轻。乙酰葛根素在高、中、低浓度下增加神经元活力。荧光检测结果显示，乙酰葛根素和MK-801治疗组在每个再灌注时间的钙浓度均有所降低。结论我们的研究结果表明，乙酰葛根素可以通过减轻形态损伤、增加神经元活力和降低神经元钙浓度来保护大鼠海马神经元免受缺血再灌注损伤。
ObjectivesThis study was undertaken to find out the effects of acetylpuerarin on hippocampal neurons and intracellular free calcium in primary culture subjected to oxygen–glucose deprivation/reperfusion.MethodsAccording to different reperfusion time (1 h, 6 h, 12 h, 24 h), three concentrations (1.6 μmol l−1, 0.4 μmol l−1, 0.1 μmol l−1) of acetylpuerarin, and MK-801 (10 μmol l−1), a positive control drug, neurons were randomly divided into 21 groups. Each group was observed by inverted phase contrast microscope; neuron viability was measured by the reduction of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT); intracellular Ca2+was observed by Fura-2/AM ester through fluorospectrophotometer.ResultsThe injured neurons were protected and degeneration and necrosis were alleviated in treatment groups of acetylpuerarin and MK-801. Acetylpuerarin increased the neuron viability at high, middle and low concentrations. Fluorescence detection results showed that the calcium concentration in the group treated with acetylpuerarin and MK-801 was lowered in each reperfusion time.ConclusionOur results demonstrated that acetylpuerarin could protect the hippocampal neurons from ischemia–reperfusion injury in rats by alleviating the morphological damage, increasing neuron viability and decreasing calcium concentration in neuron.
ONO-1603 是一种潜在的抗痴呆药物，可延缓年龄诱导的细胞凋亡，并抑制培养的中枢神经系统神经元中甘油醛-3-磷酸脱氢酶的过度表达。
DOI：
--
发表时间：
1999
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Katsube,N;Sunaga,K;Aishita,H;Chuang,DM;Ishitani,R
通讯作者：
Ishitani,R
影响因子：
2.5
作者：
B. A. Summers;J. L. Overholt;Nanduri R. Prabhakar
通讯作者：
B. A. Summers;J. L. Overholt;Nanduri R. Prabhakar