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越南人参皂苷及其主要成分人参皂苷R2对心理应激诱导的小鼠脑脂质过氧化增强的抑制作用。

Suppressive effects of vietnamese ginseng saponin and its major component majonoside-R2 on psychological stress-induced enhancement of lipid peroxidation in the mouse brain.

作者信息

Yobimoto K, Matsumoto K, Huong N T, Kasai R, Yamasaki K, Watanabe H

机构信息

Department of Pharmacology, Institute of Natural Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, 930-0194, Toyama, Japan.

出版信息

Pharmacol Biochem Behav. 2000 Jul;66(3):661-5. doi: 10.1016/s0091-3057(00)00257-4.

Abstract

We investigated the in vivo effects of Vietnamese ginseng saponin (VG saponin) and its major component majonoside-R2 (MR2) on psychological stress-induced enhancement of lipid peroxidation in the mouse brain. Psychological stress exposure using a communication box system for 4 h significantly increased the content of thiobarbituric acid reactive substance (TBARS), an index of lipid peroxidation activity, in the brain. Pretreatment with VG saponin (15-25 mg/kg, PO) and MR2 (1-10 mg/kg, IP) significantly attenuated the psychological stress-induced increase in TBARS content in the brain. The aglycone of MR2 (MR2-aglycone: 1.2 mg/kg, IP), at the equivalent dose of MR2 (i.e., 3 mg/kg, IP), also produced the suppressive effect on the increase in the TBARS content. The in vivo suppressive effect of MR2 was dose dependently attenuated by flumazenil (3 and 10 mg/kg, IP), a benzodiazepine receptor antagonist, and pregnenolone sulfate (10 mg/kg, IP), a neurosteroidal negative allosteric modulator of GABA(A) receptors. These findings suggest that VG saponin and its major component MR2 have preventive effects on the psychological stress-induced brain cell membrane damage, and that the effect of MR2 is partly due to enhancement of GABA(A)-ergic systems in the brain.

摘要

我们研究了越南人参皂苷(VG皂苷)及其主要成分人参皂苷R2(MR2)对心理应激诱导的小鼠脑内脂质过氧化增强的体内作用。使用交流箱系统进行4小时的心理应激暴露显著增加了脑内硫代巴比妥酸反应物质(TBARS)的含量,TBARS是脂质过氧化活性的指标。用VG皂苷(15 - 25毫克/千克,口服)和MR2(1 - 10毫克/千克,腹腔注射)预处理可显著减轻心理应激诱导的脑内TBARS含量增加。MR2的苷元(MR2 - 苷元:1.2毫克/千克,腹腔注射),在与MR2等效剂量(即3毫克/千克,腹腔注射)时,也对TBARS含量的增加产生抑制作用。MR2的体内抑制作用被氟马西尼(3和10毫克/千克,腹腔注射),一种苯二氮䓬受体拮抗剂,和孕烯醇酮硫酸盐(10毫克/千克,腹腔注射),一种GABA(A)受体的神经甾体负性变构调节剂,剂量依赖性地减弱。这些发现表明,VG皂苷及其主要成分MR2对心理应激诱导的脑细胞膜损伤具有预防作用,并且MR2的作用部分归因于脑内GABA(A)能系统的增强。

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