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[摘要]
本文研究了刺五加多糖抗运动性疲劳作用及与氧化应激的相关性。将小鼠随机分为对照组及刺五加多糖低、中、高剂量组,对照组小鼠灌胃蒸馏水,刺五加多糖低、中、高剂量组分别灌胃50、100及200 mg/kg的刺五加多糖,每天1次,连续给药28 d。研究结果发现,与对照组比较,刺五加多糖低、中、高剂量组小鼠给药前、末次给药后体质量及给药期间体质量增长等指标均无明显变化(P>0.05),负重游泳时间延长(P<0.01);与对照组比较,刺五加多糖低、中、高剂量组小鼠肌糖原、肝糖原含量及骨骼肌GSH-Px、SOD活性增加(P<0.05,P<0.01),BUN、乳酸、血糖、血氨及骨骼肌MDA含量降低(P<0.05,P<0.01);与对照组比较,刺五加多糖中、高剂量组小鼠骨骼肌NOX2及低、中、高剂量组NOX4、Keap1基因表达下降(P<0.05,P<0.01),而刺五加多糖各剂量组Nrf2及HO-1基因表达增加(P<0.05,P<0.01),同时相关蛋白的表达水平具有一致的趋势。以上结果表明,刺五加多糖具有抗小鼠运动性疲劳作用,该作用与抑制NOX2、NOX4表达及调节Nrf2/ARE信号通路,进而抑制氧化应激有关。
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[Abstract]
The anti-exercise fatigue effect of Acanthopanax senticosus polysaccharide (ASP) and its correlation with oxidative stress were investigated. Mice were randomly divided into control group and low-, medium- and high dose ASP groups. Mice in control group were intragastrically given distilled water, while those in low-, medium- and high dose ASP groups were intragastrically given 50, 100 and 200 mg/kg ASP once a day for consecutive 28 days, respectively. The study found that compared with control group, the body mass of mice before and after the last administration and the increase of body mass during administration in low-, medium- and high dose ASP groups had no significant changes (P>0.05), and the weight-bearing swimming time was prolonged (P<0.01); compared with control group, the glycogen contents in muscle and liver and the activities of GSH-Px and SOD in low-, medium- and high dose ASP groups were increased (P<0.05, P<0.01), while the contents of BUN, lactic acid, blood glucose, blood ammonia and MDA were decreased (P<0.05, P<0.01); compared with control group, NOX2 gene expression in skeletal muscle of mice in medium- and high dose ASP groups and NOX4 and Keap1 gene expressions in low-, medium- and high dose ASP groups were decreased (P<0.05, P<0.01), while Nrf2 and HO-1 gene expressions in each dose ASP group were increased (P<0.05, P<0.01), meanwhile, the expression levels of related proteins showed a consistent trend. The above results indicate that ASP has the effect of anti-exercise fatigue in mice, which is related to the inhibition of NOX2 and NOX4 expressions and the regulation of Nrf2/ARE signaling pathway, and then the inhibition of oxidative stress.
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