摘要
苦丁冬青苷D是大叶冬青苦丁茶中的主要生物活性物质,具有多种生物活性。本研究旨在探究苦丁茶树中的主要生物活性物质苦丁冬青苷D在力竭运动肥胖大鼠中的作用及其潜在机制。将肥胖大鼠随机分为不同处理组和正常对照组,通过灌胃给予苦丁冬青苷D不同剂量,并观察力竭游泳时间、血脂代谢、心肌损伤、氧化应激反应以及骨骼肌和心肌AMPK通路的变化。结果显示,未经处理的肥胖大鼠表现出较长的力竭游泳时间、异常的血脂代谢、增加的心肌损伤以及升高的氧化应激反应水平,同时骨骼肌和心肌AMPK通路受到抑制。然而,在苦丁冬青苷D干预下,力竭游泳时间显著增加,血脂代谢异常得到改善,心肌损伤减轻,氧化应激反应水平下降,同时骨骼肌和心肌AMPK通路得到激活。本研究初步得出结论:苦丁冬青苷D通过调节肥胖大鼠的血脂代谢、心肌损伤、氧化应激反应以及骨骼肌和心肌AMPK通路的活性,对力竭运动肥胖大鼠产生积极影响。这些结果为进一步研究苦丁冬青苷D的药理作用和临床应用提供了重要线索。
Kudinoside D,a major bioactive compound found in Ilex latifolia,possesses diverse biological activities.This study aimed to investigate the effects and potential mechanisms of kudinoside D on exhaustive exercise-induced obesity in rats.Obese rats were randomly assigned to different treatment groups,along with a normal control group.Various doses of kudinoside D were administered via oral gavage,and the changes in exhaustive swimming time,lipid metabolism,myocardial injury,oxidative stress response,and skeletal muscle and myocardial AMPK pathways were observed.The results demonstrated that untreated obese rats exhibited prolonged exhaustive swimming time,abnormal lipid metabolism,increased myocardial injury,elevated oxidative stress response,and suppressed skeletal muscle and myocardial AMPK pathways compared to the control group.However,intervention with kudinoside D significantly increased exhaustive swimming time,improved lipid metabolism abnormalities,alleviated myocardial injury,reduced oxidative stress response,and activated skeletal muscle and myocardial AMPK pathways.In conclusion,kudinoside D exerts positive effects on exhaustive exercise-induced obesity in rats by modulating lipid metabolism,myocardial injury,oxidative stress response,and the activity of skeletal muscle and myocardial AMPK pathways.These findings provide important insights for further exploring the pharmacological effects and clinical applications of kudinoside D.
作者
李敏
Li Min(School of Physical Education,Qingdao University,Qingdao,266071)
出处
《分子植物育种》
CAS
北大核心
2023年第14期4780-4787,共8页
Molecular Plant Breeding
基金
青岛大学科研基金项目资助。