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云芝多糖减轻半乳糖诱导的小鼠脑氧化应激。

Ganoderma atrum polysaccharide attenuates oxidative stress induced by d-galactose in mouse brain.

机构信息

State Key Laboratory of Food Science and Technology, Nanchang University, Nanchang 330047, China.

出版信息

Life Sci. 2011 Apr 11;88(15-16):713-8. doi: 10.1016/j.lfs.2011.02.010. Epub 2011 Feb 18.

DOI:10.1016/j.lfs.2011.02.010
PMID:21334348
Abstract

AIMS

Ganoderma atrum polysaccharide (PSG-1), the main constituent of G. atrum, has been reported to attenuate oxidative stress in vitro. The aim of this study was to investigate whether PSG-1 has a protective effect on the brain against oxidative stress induced by D-galactose (D-gal) in vivo.

MAIN METHODS

Mice were intraperitoneally (i.p.) injected with D-gal (100 mg/kg body weight) once daily for 10 weeks. From the seventh week, D-gal-treated mice received PSG-1 (50, 100, or 150 mg/kg body weight) once daily for the last 4 weeks. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GSH-Rd), and the contents of glutathione (GSH), glutathione disulfide (GSSG) and malondialdehyde (MDA) in the brain were measured using different biochemical methods to evaluate the changes of the antioxidant ability in the PSG-1 treated mice. Apoptosis, reactive oxygen species (ROS) and calcium levels were determined by flow cytometry.

KEY FINDINGS

Administration of PSG-1 significantly reduced apoptosis in the mouse brain in a dose-dependent manner. PSG-1-evoked reduction of apoptosis was associated with the decrease of MDA and GSSG contents, and the increase of SOD, CAT, GPx and GSH-Rd activities, and GSH contents. PSG-1 treatment was also found to attenuate ROS production and calcium accumulation.

SIGNIFICANCE

PSG-1 has a potential to be used as a novel therapeutic agent for the protection of aging brain tissue against oxidative damage by modifying the redox system and maintaining calcium homeostasis.

摘要

目的

赤芝多糖(PSG-1)是赤芝的主要成分,已被报道可减轻体外氧化应激。本研究旨在探讨 PSG-1 是否对体内 D-半乳糖(D-gal)诱导的大脑氧化应激具有保护作用。

主要方法

小鼠腹腔内(i.p.)注射 D-gal(100mg/kg 体重),每天 1 次,共 10 周。从第 7 周开始,D-gal 处理的小鼠连续 4 周每天接受 PSG-1(50、100 或 150mg/kg 体重)治疗。使用不同的生化方法测量大脑中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽还原酶(GSH-Rd)的活性以及谷胱甘肽(GSH)、谷胱甘肽二硫化物(GSSG)和丙二醛(MDA)的含量,以评估 PSG-1 处理小鼠抗氧化能力的变化。通过流式细胞术测定细胞凋亡、活性氧(ROS)和钙水平。

主要发现

PSG-1 以剂量依赖的方式显著减少了小鼠大脑中的细胞凋亡。PSG-1 诱导的细胞凋亡减少与 MDA 和 GSSG 含量的降低,以及 SOD、CAT、GPx 和 GSH-Rd 活性和 GSH 含量的增加有关。PSG-1 治疗还可减弱 ROS 生成和钙积累。

意义

PSG-1 有潜力通过调节氧化还原系统和维持钙稳态,成为保护衰老脑组织免受氧化损伤的新型治疗剂。

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