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中国精品科技期刊2020
郑传痴,杨艳,韦余,等. 金丝桃苷对小鼠的抗疲劳作用及机制研究[J]. 食品工业科技,2021,42(23):350−355. doi: 10.13386/j.issn1002-0306.2021010227.
引用本文: 郑传痴,杨艳,韦余,等. 金丝桃苷对小鼠的抗疲劳作用及机制研究[J]. 食品工业科技,2021,42(23):350−355. doi: 10.13386/j.issn1002-0306.2021010227.
ZHENG Chuanchi, YAN Yan, WEI Yu, et al. Study on the Effects and Mechanism of Hyperoside on Anti-Fatigue in Mice[J]. Science and Technology of Food Industry, 2021, 42(23): 350−355. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021010227.
Citation: ZHENG Chuanchi, YAN Yan, WEI Yu, et al. Study on the Effects and Mechanism of Hyperoside on Anti-Fatigue in Mice[J]. Science and Technology of Food Industry, 2021, 42(23): 350−355. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2021010227.

金丝桃苷对小鼠的抗疲劳作用及机制研究

Study on the Effects and Mechanism of Hyperoside on Anti-Fatigue in Mice

  • 摘要: 研究金丝桃苷的抗疲劳作用及其作用机制。将小鼠随机分为空白对照组、金丝桃苷低(5 mg/kg)、中(10 mg/kg)、高(20 mg/kg)剂量组,通过转棒实验和力竭游泳实验评价金丝桃苷的抗疲劳能力;通过酶联免疫吸附测定法检测小鼠的血乳酸(lactic acid, LA)、血尿素氮(blood urea nitrogen, BUN)、肝糖原(liver glycogen, LG)、肌糖原(muscle glycogen, MG)、肝组织中活性氧(reactive oxygen species, ROS)、丙二醛(malondialdehyde, MDA)、超氧化物歧化酶(superoxide dismutase, SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase, GSH-Px)等疲劳相关生化指标和氧化应激相关指标。通过分子对接技术分析和Western blot法分别检测金丝桃苷与核因子E2相关因子(nuclear factor erythroid 2-related factor 2, Nrf2)蛋白的结合情况及Nrf2信号途径相关蛋白血红素加氧酶1(heme oxygenase 1, HO-1)、NADPH醌氧化还原酶1(NADPH quinone oxidoreductase 1, NQO1)的表达。结果表示,与空白对照组比较,金丝桃苷(5、10、20 mg/kg)能够剂量依赖性的显著延长小鼠的转棒停留时间和力竭游泳时间(P<0.05),显著降低小鼠LA和BUN的含量,增加LG和MG的含量(P<0.05);与空白对照组比较,金丝桃苷能够明显减少ROS和MDA含量,增加SOD和GSH-Px的活力(P<0.05);金丝桃苷与Nrf2的对接能量为−11.21 kcal/mol,提示Nrf2可能是金丝桃苷的潜在作用靶点。金丝桃苷能够增加胞核Nrf2的蛋白水平,上调HO-1和NQO-1的蛋白表达。以上结果表明,金丝桃苷能够通过调控Nrf2信号途径提高机体的抗氧化能力进而发挥其抗疲劳作用。

     

    Abstract: The present study was designed to explore the effects and mechanism of hyperoside on anti-fatigue in mice. The mice were randomly divided into four groups, including the control group, low-dose (5 mg/kg) hyperoside group, medium-dose (10 mg/kg) hyperoside group and high-dose (20 mg/kg) hyperoside group. The rotating rod test and exhaustive swimming test were used to determine the anti-fatigue effect of hyperoside. Then, the lactic acid (LA), blood urea nitrogen (BUN), liver glycogen (LG), muscle glycogen (MG), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were measured using enzyme-linked immunosorbent assay. There after, the binding energy between hyperoside and nuclear factor erythroid 2-related factor 2 (Nrf2), and the protein expressions of Nrf2, heme oxygenase 1 (HO-1), NADPH quinone oxidoreductase 1 (NQO1) were detected by molecular docking and Western blot, respectively. The results showed that hyperoside (5, 10, 20 mg/kg) significantly increased the rotating rod lasting time and the exhaustive swimming time in mice than those of control group (P<0.05). Moreover, hyperoside markedly reduced the contents of LA and BUN, while increased the contents of LG and MG in mice than those of control group (P<0.05); hyperoside also obviously decreased the contents of ROS and MDA, increased the activities of SOD and GSH-Px in mice than those of control group (P<0.05). Of note, the binding energy of hyperoside with Nrf2 was −11.21 kcal/mol, which indicated that Nrf2 might be the potential target of hyperoside. Furthermore, hyperoside increased the level of Nrf2 in nucleus, as well as up-regulated the protein expressions of HO-1 and NQO-1. These findings suggested that hyperoside exerted anti-fatigue effect and antioxidative activity through mediating Nrf2 signaling pathway.

     

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