基于氧化应激研究刺五加多糖的抗运动性疲劳作用

该文研究了ASP（刺五加多糖）的抗运动性疲劳与抑制氧化应激作用。将小鼠随机分为对照组及刺五加多糖低、中、高剂量组（50、100、200 mg/kg），连续干预28 d。结果发现，与对照组比较，刺五加多糖低、中、高剂量组小鼠负重游泳时间延长了13.79%、33.68%和48.89%，肌糖原、肝糖原含量增加，BUN（血尿素氮）、乳酸、血糖及血氨含量降低；与对照组比较，刺五加多糖低、中、高剂量组小鼠骨骼肌GSH-Px（谷胱甘肽过氧物酶）活性增加了29.82%、53.03%和59.32%,SOD（超氧化物歧化酶）活性增加了9.64%、15.23%和50.05%,MDA（丙二醛）含量降低了16.45%、36.76%和45.82%；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，而刺五加多糖各剂量组Nrf2及HO-1基因表达增加，同时相关蛋白的表达水平具有一致的趋势。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，进而抑制氧化应激作用有关。

Anti-exercise-fatigue Effect of Acanthopanax senticosus Polysaccharide Based on Oxidative Stress

The anti-exercise-fatigue and oxidative stress inhibitory effects of Acanthopanax senticosus polysaccharide (ASP) was investigated. Mice were randomly divided into the control group and the low-, medium- and high dose ASP groups (50, 100 and 200 mg/kg), and the intervention lasted for 28 days. The results showed that compared with the control group, the weight-bearing swimming times of mice for the low-, medium- and high dose ASP groups were prolonged by 13.79%, 33.68% and 48.89%, respectively, the contents of muscle glycogen and liver glycogen increased, and the contents of BUN, lactic acid, blood glucose and blood ammonia decreased; Compared with the control group, the activity of GSH-Px in the skeletal muscle for the low-, medium- and high dose ASP mice increased by 29.82%, 53.03% and 59.32%, respectively, their SOD activities increased by 9.64%, 15.23% and 50.05%, respectively, and their MDA contents decreased by 16.45%, 36.76% and 45.82%, respectively; Compared with the control group, NOX2 gene expression in the skeletal muscle of the medium- and high dose ASP groups and the NOX4 and Keap1 gene expressions of the low-, medium- and high dose ASP groups decreased, whilst Nrf2 and HO-1 gene expressions of all the ASP groups increased, and the expression levels of related proteins showed a consistent trend. The results showed that ASP has an anti-exercise-fatigue effect in mice, which is related to the inhibition of NOX2 and NOX4 expressions and the regulation of Nrf2/ARE signaling pathway, thereby inhibiting oxidative stress.