山东科学 ›› 2024, Vol. 37 ›› Issue (6): 51-58.doi: 10.3976/j.issn.1002-4026.20240034

• 药理与毒理 • 上一篇    下一篇

基于PI3K/AKT/Gsk-3β通路研究山药多糖对运动疲劳小鼠的影响

曾婷1(), 杨然1, 李庆军1, 宫亚楠2, 王书珍1,3,*(), 刘谦1,*()   

  1. 1.山东中医药大学 药学院,山东 济南 250355
    2.济南市章丘区人民医院 心内一科,山东 济南 250299
    3.黄冈师范学院 生物与农业资源学院,湖北 黄冈 438000
  • 收稿日期:2024-03-06 出版日期:2024-12-20 发布日期:2024-12-05
  • 通信作者: *刘谦,女,教授,博士,研究方向为中药资源与可持续利用研究。E-mail:cleanlq@163.com, Tel:13290326687; 王书珍,女,博士,副教授,研究方向为中草药生物活性成分作用机制及活性成分鉴定研究。E-mail:wangshuzhen710@whu.edu.cn, Tel:18171758890
  • 作者简介:曾婷(1998—),女,硕士研究生,研究方向为中草药生物活性成分作用机制及活性成分鉴定研究。E-mail:2452280058@qq.com
  • 基金资助:
    山东省重点研发计划项目(2021CXGC010510);财政部和农业农村部:国家现代农业产业技术体系项目(CARS-21);国家自然科学基金项目(82003892);泰山学者工程专项经费资助项目(tsqn202306187);中央引导地方科技发展资金项目(XZ202301YD0023C)

Effects of Dioscorea opposita Thunb. polysacchariades on exercise-related fatigue in mice through the PI3K/AKT/Gsk-3β pathway

ZENG Ting1(), YANG Ran1, LI Qingjun1, GONG Yanan2, WANG Shuzhen1,3,*(), LIU Qian1,*()   

  1. 1. College of Pharmacy, Shandong University of Traditional Chinese Medicine, Jinan 250355, China
    2. The First Department of Cardiology, Jinan Zhangqiu District People's Hospital, Jinan 250299, China
    3. College of Biology and Agricultural Resources, Huanggang Normal University, Huanggang 438000, China
  • Received:2024-03-06 Online:2024-12-20 Published:2024-12-05

摘要:

研究山药多糖(Dioscorea opposita Thunb. polysaccharides,DTPs)对运动疲劳小鼠的抗疲劳作用及作用机制。采用力竭游泳结合疲劳转棒方法建立小鼠运动疲劳模型,分析小鼠力竭游泳时间和体重变化、疲劳代谢产物积累、相关酶活力水平、肝脏组织结构和肌肝糖原变化。结果表明:山药多糖能显著延长小鼠力竭游泳时间,减轻小鼠体重下降和肝脏损伤,显著降低血清乳酸(LD)、尿素氮(BUN)、乳酸脱氢酶(LDH)含量并显著提高超氧化物歧化酶(SOD)活力及肌糖原(MuG)和肝糖原(LG)含量,同时显著降低谷草转氨酶(AST)水平;此外,给药组显著上调骨骼肌中磷脂酰肌醇3-激酶(Phosphoinositide 3-kinase,PI3K)mRNA表达、显著降低蛋白激酶B(Protein kinase B,AKT)和糖原合成酶激酶-3(Glycogen synthase kinase-3 beta,Gsk-3β)的表达。综上,山药多糖能减少代谢产物积累、通过调节PI3K/AKT/Gsk-3β通路促进糖原合成来改善运动疲劳。

关键词: 山药多糖, 抗运动疲劳, 力竭游泳, PI3K/AKT/Gsk-3β通路

Abstract:

This study aimed to investigate the antifatigue effects and mechanisms of Dioscorea opposita Thunb. polysaccharides (DTPs) on exercise-related fatigue in mice. In a mouse model of exercise fatigue where mice were subjected to exhaustive swimming and fatigue rotarod, changes in exhaustive swimming duration, body weight, fatigue metabolite accumulation, activity levels of related enzymes, liver tissue structure, and muscle glycogen (MuG) and liver glycogen (LG) contents were assessed. The results demonstrated that DTPs significantly prolonged the exhaustive swimming duration and reduced body weight loss, hepatic damage, and serum lactic acid (LD), blood urea nitrogen (BUN), and lactate dehydrogenase (LDH) levels in the mice. DTPs also significantly enhanced superoxide dismutase (SOD) activity and MuG and LG contents and significantly reduced aspartate aminotransferase (AST) levels. Additionally, in mice administered DTPs, the mRNA expression of phosphoinositide 3-kinase (PI3K) was significantly upregulated, whereas that of protein kinase B (AKT) and glycogen synthase kinase-3 (Gsk-3β) was significantly downregulated in skeletal muscle. Taken together, DTPs can reduce metabolite accumulation and ameliorate exercise fatigue by regulating the PI3K/AKT/Gsk-3β pathway to promote glycogen synthesis.

Key words: Dioscorea opposita Thunb. polysaccharides, anti-exercise fatigue, exhaustive swimming, PI3K/AKT/Gsk-3β pathway

中图分类号: 

  • R96

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