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中国精品科技期刊2020
高泽谨,康姮,宋巧. 甜叶菊糖苷对过度运动疲劳大鼠肝脏线粒体能量代谢和氧化应激的影响[J]. 华体会体育,2025,46(6):1−10. doi: 10.13386/j.issn1002-0306.2024060016.
引用本文: 高泽谨,康姮,宋巧. 甜叶菊糖苷对过度运动疲劳大鼠肝脏线粒体能量代谢和氧化应激的影响[J]. 华体会体育,2025,46(6):1−10. doi: 10.13386/j.issn1002-0306.2024060016.
GAO Zejin, KANG Xi, SONG Qiao. Effects of Steviol Glycosides on Mitochondrial Energy Metabolism and Oxidative Stress in Liver of Rats with Excessive Exercise Fatigue[J]. Science and Technology of Food Industry, 2025, 46(6): 1−10. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024060016.
Citation: GAO Zejin, KANG Xi, SONG Qiao. Effects of Steviol Glycosides on Mitochondrial Energy Metabolism and Oxidative Stress in Liver of Rats with Excessive Exercise Fatigue[J]. Science and Technology of Food Industry, 2025, 46(6): 1−10. (in Chinese with English abstract). doi: 10.13386/j.issn1002-0306.2024060016.

甜叶菊糖苷对过度运动疲劳大鼠肝脏线粒体能量代谢和氧化应激的影响

Effects of Steviol Glycosides on Mitochondrial Energy Metabolism and Oxidative Stress in Liver of Rats with Excessive Exercise Fatigue

  • 摘要: 目的:以甜叶菊叶片为实验材料,提取分离得到甜叶菊糖苷(Stevia glycoside,SG),探讨其对过度运动疲劳大鼠肝脏线粒体能量代谢和氧化应激的影响。方法:采用高效液相色谱法分析甜叶菊糖苷单体组成。将大鼠随机分为安静对照组(SC)、运动疲劳模型组(EC)、甜菊糖苷低剂量组(SG-L,50 mg/kg)、中剂量组(SG-M,100 mg/kg)、高剂量组(SG-H,200 mg/kg),灌胃体积为20 mL/kg,通过连续5周游泳实验建立大鼠过度运动疲劳模型,检测大鼠生理生化代谢指标和线粒体内相关酶活性;同时检测肝脏能量代谢信号通路中AMPKPGC-1αTFAMSIRT1基因mRNA表达水平。结果:甜叶菊中总糖苷占比17.82%,其中甜菊糖苷中甜菊苷占比最大(24.26%),瑞鲍迪苷B占比最少(0.38%)。与EC相比,低、中、高剂量甜菊糖苷均显著提高了大鼠糖原储备,肝糖原、肌糖原含量分别显著提高了12.34%、56.07%、91.42%(P<0.05)和33.77%、76.62%、131.17%(P<0.05),血乳酸、血尿素氮含量分别显著降低了16.75%、31.19%、44.81%和19.42%、28.42%、40.38%(P<0.05),同时大鼠肝脏线粒体ATP酶、呼吸链酶复合物(CⅠ~Ⅳ)、抗氧化酶活性均显著提高(P<0.05),丙二醛含量则显著降低(P<0.05),且均呈现剂量依赖性。此外,补充甜菊糖苷激活了肝脏AMPK/PGC-1α能量代谢调控通路,与EC相比,SG-L、SG-M、SG-H均显著提高了AMPKPGC-1αTFAMSIRT1的mRNA表达水平(P<0.05)。结论:甜叶菊糖苷可通过激活AMPK/PGC-1α信号通路,促进肝脏线粒体能量代谢,提高ATP的生成,从而提高大鼠的抗疲劳作用,同时甜叶菊糖苷还具有降低肝脏线粒体氧化应激水平的作用,进而缓解大鼠的运动疲劳。

     

    Abstract: Objective: Using Stevia rebaudiana leaves as experimental materials, stevia glycoside (SG) was extracted and isolated, and its effects on mitochondrial energy metabolism and oxidative stress in the liver of rats with excessive exercise fatigue were investigated. Methods: High-performance liquid chromatography was used to analyze the monomer composition of Stevia glycosides. Rats were randomly divided into a sedentary control group (SC), an exercise-induced fatigue model group (EC), a low-dose Stevia glycoside group (SG-L, 50 mg/kg), a medium-dose group (SG-M, 100 mg/kg), and a high-dose group (SG-H, 200 mg/kg). Rats were orally gavaged with 20 mL/kg and an exercise-induced fatigue model was established through 5 weeks of swimming experiments. Physiological and biochemical metabolic indicators and mitochondrial enzyme activities in rats were measured. Additionally, mRNA expression levels of AMPK, PGC-1α, TFAM, and SIRT1 genes in the hepatic energy metabolism signaling pathway were evaluated. Results: Steviol glycosides accounted for 17.82% of the total glycosides in stevia rebaudiana leaves, with steviol glycoside having the highest proportion (24.26%) and rebaudioside B having the lowest proportion (0.38%). Compared with EC, low, medium, and high doses of stevia glycosides significantly increased glycogen reserves in rat, the hepatic glycogen and muscle glycogen contents were significantly increased by 12.34%, 56.07%, 91.42% (P<0.05) and 33.77%, 76.62%, 131.17% (P<0.05), respectively. Blood lactate and blood urea nitrogen levels were significantly reduced by 16.75%, 31.19%, 44.81% and 19.42%, 28.42%, 40.38% (P<0.05), respectively. Hepatic mitochondrial ATPase, respiratory chain enzyme complexes (CⅠ−Ⅳ), and antioxidant enzyme activities were significantly increased (P<0.05), while malondialdehyde content was significantly decreased (P<0.05), all showing dose-dependency. Furthermore, supplementation with stevia glycosides activated the hepatic AMPK/PGC-1α energy metabolism regulatory pathway. Compared to EC, SG-L, SG-M, and SG-H significantly increased the mRNA expression levels of AMPK, PGC-1α, TFAM, and SIRT1 (P<0.05). Conclusion: Stevia glycosides can promote hepatic mitochondrial energy metabolism by activating the AMPK/PGC-1α signaling pathway, increasing ATP production, enhancing the anti-fatigue effect in rats, and also reducing hepatic mitochondrial oxidative stress levels, thereby alleviating exercise-induced fatigue in rats.

     

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