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本文引用的文献

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Ginsenoside Rd attenuates mitochondrial dysfunction and sequential apoptosis after transient focal ischemia.人参皂苷 Rd 减轻短暂性局灶性缺血后线粒体功能障碍和序贯性细胞凋亡。
Neuroscience. 2011 Mar 31;178:169-80. doi: 10.1016/j.neuroscience.2011.01.007. Epub 2011 Jan 8.
2
Ginsenoside Rd attenuates early oxidative damage and sequential inflammatory response after transient focal ischemia in rats.人参皂苷 Rd 减轻大鼠短暂性局灶性缺血后早期氧化损伤和序贯性炎症反应。
Neurochem Int. 2011 Feb;58(3):391-8. doi: 10.1016/j.neuint.2010.12.015. Epub 2010 Dec 24.
3
Hypolipidemic and antioxidant activities of sanchi (radix notoginseng) in rats fed with a high fat diet.高脂饮食大鼠桑枝(三七)的降血脂和抗氧化活性。
Phytomedicine. 2011 Apr 15;18(6):516-20. doi: 10.1016/j.phymed.2010.09.007. Epub 2010 Oct 30.
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Calcium, ischemia and excitotoxicity.钙、缺血和兴奋毒性。
Cell Calcium. 2010 Feb;47(2):122-9. doi: 10.1016/j.ceca.2010.01.003. Epub 2010 Feb 18.
5
Ginsenoside Rd prevents glutamate-induced apoptosis in rat cortical neurons.人参皂苷 Rd 可预防谷氨酸诱导的大鼠皮质神经元细胞凋亡。
Clin Exp Pharmacol Physiol. 2010 Feb;37(2):199-204. doi: 10.1111/j.1440-1681.2009.05286.x. Epub 2009 Aug 28.
6
Neuroprotective effects of ginsenoside Rd against oxygen-glucose deprivation in cultured hippocampal neurons.人参皂苷Rd对培养海马神经元氧糖剥夺的神经保护作用。
Neurosci Res. 2009 Jul;64(3):306-10. doi: 10.1016/j.neures.2009.03.016. Epub 2009 Apr 10.
7
Ginsenoside-Rd, a new voltage-independent Ca2+ entry blocker, reverses basilar hypertrophic remodeling in stroke-prone renovascular hypertensive rats.人参皂苷-Rd,一种新型的非电压依赖性Ca2+通道阻滞剂,可逆转易卒中型肾血管性高血压大鼠的基底动脉肥厚性重塑。
Eur J Pharmacol. 2009 Mar 15;606(1-3):142-9. doi: 10.1016/j.ejphar.2009.01.033. Epub 2009 Jan 29.
8
Efficacy and safety of ginsenoside-Rd for acute ischaemic stroke: a randomized, double-blind, placebo-controlled, phase II multicenter trial.人参皂苷-Rd治疗急性缺血性脑卒中的疗效和安全性:一项随机、双盲、安慰剂对照的II期多中心试验。
Eur J Neurol. 2009 May;16(5):569-75. doi: 10.1111/j.1468-1331.2009.02534.x. Epub 2009 Feb 19.
9
Native and recombinant ASIC1a receptors conduct negligible Ca2+ entry.天然和重组ASIC1a受体介导的钙离子内流可忽略不计。
Cell Calcium. 2009 Apr;45(4):319-25. doi: 10.1016/j.ceca.2008.12.002. Epub 2009 Jan 29.
10
Long-term ginsenoside consumption prevents memory loss in aged SAMP8 mice by decreasing oxidative stress and up-regulating the plasticity-related proteins in hippocampus.长期服用人参皂苷可通过降低氧化应激和上调海马体中与可塑性相关的蛋白质来预防衰老的SAMP8小鼠的记忆丧失。
Brain Res. 2009 Feb 23;1256:111-22. doi: 10.1016/j.brainres.2008.12.031. Epub 2008 Dec 24.

人参皂苷 Rd 通过抑制 Ca(2+)内流保护神经元免受谷氨酸诱导的兴奋性毒性。

Ginsenoside Rd protects neurons against glutamate-induced excitotoxicity by inhibiting ca(2+) influx.

机构信息

Department of Neurology, Xijing Hospital, The Fourth Military Medical University, 15 Changle Xi Road, Xi'an, 710032, China.

出版信息

Cell Mol Neurobiol. 2012 Jan;32(1):121-8. doi: 10.1007/s10571-011-9742-x. Epub 2011 Aug 3.

DOI:10.1007/s10571-011-9742-x
PMID:21811848
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11498599/
Abstract

Our previous studies have demonstrated that ginsenoside Rd (GSRd), one of the principal ingredients of Pana notoginseng, has neuroprotective effects against ischemic stroke. However, the possible mechanism(s) underlying the neuroprotection of GSRd is/are still largely unknown. In this study, we treated glutamate-injured cultured rat hippocampal neurons with different concentrations of GSRd, and then examined the changes in neuronal apoptosis and intracellular free Ca(2+) concentration. Our MTT assay showed that GSRd significantly increased the survival of neurons injured by glutamate in a dose-dependent manner. Consistently, TUNEL and Caspase-3 staining showed that GSRd attenuated glutamate-induced cell death. Furthermore, calcium imaging assay revealed that GSRd significantly attenuated the glutamate-induced increase of intracellular free Ca(2+) and also inhibited NMDA-triggered Ca(2+) influx. Thus, the present study demonstrates that GSRd protects the cultured hippocampal neurons against glutamate-induced excitotoxicity, and that this neuroprotective effect may result from the inhibitory effects of GSRd on Ca(2+) influx.

摘要

我们之前的研究表明,三七总皂苷(GSRd)是三七的主要成分之一,具有抗缺血性中风的神经保护作用。然而,GSRd 的神经保护作用的可能机制在很大程度上仍然未知。在这项研究中,我们用不同浓度的 GSRd 处理谷氨酸损伤的培养大鼠海马神经元,然后检测神经元凋亡和细胞内游离 Ca(2+)浓度的变化。我们的 MTT 检测显示,GSRd 以剂量依赖的方式显著增加了谷氨酸损伤神经元的存活率。同样,TUNEL 和 Caspase-3 染色显示 GSRd 减轻了谷氨酸诱导的细胞死亡。此外,钙成像检测显示,GSRd 显著减轻了谷氨酸诱导的细胞内游离 Ca(2+)增加,并抑制了 NMDA 触发的 Ca(2+)内流。因此,本研究表明 GSRd 可保护培养的海马神经元免受谷氨酸诱导的兴奋性毒性,这种神经保护作用可能是由于 GSRd 抑制 Ca(2+)内流所致。