Department of Neurology, Xijing Hospital, The Fourth Military Medical University, 15 Changle Xi Road, Xi'an, 710032, China.
Cell Mol Neurobiol. 2012 Jan;32(1):121-8. doi: 10.1007/s10571-011-9742-x. Epub 2011 Aug 3.
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.
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。