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人参皂苷Rb1和Rg3可保护培养的大鼠皮质细胞免受谷氨酸诱导的神经退行性变。

Ginsenosides Rb1 and Rg3 protect cultured rat cortical cells from glutamate-induced neurodegeneration.

作者信息

Kim Y C, Kim S R, Markelonis G J, Oh T H

机构信息

College of Pharmacy, Seoul National University, Korea.

出版信息

J Neurosci Res. 1998 Aug 15;53(4):426-32. doi: 10.1002/(SICI)1097-4547(19980815)53:4<426::AID-JNR4>3.0.CO;2-8.

Abstract

Certain natural products and Asian herbal remedies have been used in Asia to attenuate neurodegenerative diseases, including senile dementia. We have examined derivatives of several natural products for potential neuroprotective activity in an in vitro test system. In the present study, we assayed a number of compounds that were isolated from Panax ginseng C.A. Meyer (Araliaceae) for an ability to protect rat cortical cell cultures from the deleterious effects of the neurotoxicant, glutamate. We found that ginsenosides Rb1 and Rg3 significantly attenuated glutamate-induced neurotoxicity. Brief exposure of cultures to excess glutamate caused extensive neuronal death. Glutamate-induced neuronal cell damage was reduced significantly by pretreatment with Rb1 and Rg3. Ginsenosides Rb1 and Rg3 inhibited the overproduction of nitric oxide, which routinely follows glutamate neurotoxicity, and preserved the level of superoxide dismutase in glutamate-treated cells. Furthermore, in cultures treated with glutamate, these ginsenosides inhibited the formation of malondialdehyde, a compound that is produced during lipid peroxidation, and diminished the influx of calcium. These results show that ginsenosides Rb1 and Rg3 exerted significant neuroprotective effects on cultured cortical cells. Therefore, these compounds may be efficacious in protecting neurons from oxidative damage that is produced by exposure to excess glutamate.

摘要

在亚洲,某些天然产物和亚洲草药疗法已被用于减轻包括老年痴呆症在内的神经退行性疾病。我们在体外测试系统中检测了几种天然产物的衍生物的潜在神经保护活性。在本研究中,我们测定了从五加科人参(Panax ginseng C.A. Meyer)中分离出的多种化合物保护大鼠皮质细胞培养物免受神经毒素谷氨酸有害影响的能力。我们发现人参皂苷Rb1和Rg3能显著减轻谷氨酸诱导的神经毒性。将培养物短暂暴露于过量谷氨酸会导致大量神经元死亡。用Rb1和Rg3预处理可显著降低谷氨酸诱导的神经元细胞损伤。人参皂苷Rb1和Rg3抑制了通常伴随谷氨酸神经毒性的一氧化氮过量产生,并维持了谷氨酸处理细胞中超氧化物歧化酶的水平。此外,在用谷氨酸处理的培养物中,这些人参皂苷抑制了脂质过氧化过程中产生的丙二醛的形成,并减少了钙的内流。这些结果表明,人参皂苷Rb1和Rg3对培养的皮质细胞具有显著的神经保护作用。因此,这些化合物可能在保护神经元免受因暴露于过量谷氨酸而产生的氧化损伤方面有效。

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