Huong Nguyen Thi Thu, Murakami Yukihisa, Tohda Michihisa, Watanabe Hiroshi, Matsumoto Kinzo
Division of Medicinal Pharmacology, Institute of Natural Medicines, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama 930-0194, Japan.
Biol Pharm Bull. 2005 Aug;28(8):1389-93. doi: 10.1248/bpb.28.1389.
Stressors with a physical factor such as immobilization, electric foot shock, cold swim, etc., have been shown to produce oxidative damage to membrane lipids in the brain. In this study, we investigated the effect of protracted social isolation stress on lipid peroxidation activity in the mouse brain and elucidated the protective effect of majonoside-R2, a major saponin component of Vietnamese ginseng, in mice exposed to social isolation stress. Thiobarbituric acid reactive substance levels, one of the end products of lipid peroxidation reaction, were increased in the brains of mice subjected to 6-8 weeks of social isolation stress. Measurements of nitric oxide (NO) metabolites (NO(x)(-)) also revealed a significant increase of NO production in the brains of socially isolated mice. Moreover, the depletion of brain glutathione content, an endogenous antioxidant, in socially isolated animals occurred in association with the rise in lipid peroxidation. The intraperitoneal administration of majonoside-R2 (10-50 mg/kg) had no effect on thiobarbituric acid reactive substances (TBARS), NO, or glutathione levels in the brains of group-housed control mice but it significantly suppressed the increase in TBARS and NO levels and the decrease in glutathione levels caused by social isolation stress. These results suggest that mice subjected to 6-8 weeks of social isolation stress produces oxidative damage in the brain partly via enhancement of NO production, and that majonoside-R2 exerts a protective effect by modulating NO and glutathione systems in the brain.
诸如固定不动、足部电击、冷水游泳等具有物理因素的应激源已被证明会对大脑中的膜脂质产生氧化损伤。在本研究中，我们调查了长期社会隔离应激对小鼠大脑脂质过氧化活性的影响，并阐明了越南人参的主要皂苷成分人参皂苷R2对遭受社会隔离应激的小鼠的保护作用。脂质过氧化反应的终产物之一硫代巴比妥酸反应性物质水平在遭受6 - 8周社会隔离应激的小鼠大脑中有所升高。对一氧化氮（NO）代谢产物（NO(x)(-)）的测量还显示，社会隔离小鼠大脑中的NO生成显著增加。此外，社会隔离动物大脑中内源性抗氧化剂谷胱甘肽含量的减少与脂质过氧化的增加有关。腹腔注射人参皂苷R2（10 - 50毫克/千克）对群居对照小鼠大脑中的硫代巴比妥酸反应性物质（TBARS）、NO或谷胱甘肽水平没有影响，但它显著抑制了社会隔离应激引起的TBARS和NO水平的升高以及谷胱甘肽水平的降低。这些结果表明，遭受6 - 8周社会隔离应激的小鼠部分通过增强NO生成在大脑中产生氧化损伤，并且人参皂苷R2通过调节大脑中的NO和谷胱甘肽系统发挥保护作用。
