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灵芝三萜补充剂通过调控Keap1/Nrf2/HO-1信号通路对力竭运动小鼠心肌损伤的保护作用

Protective Effects of Ganoderma Triterpenoids Supplementation Against Myocardial Injury in Exhaustion Exercise Mice via Regulation of the Keap1/Nrf2/HO-1 Pathway.

作者信息

Li Jingrong, Zhang Ling, Qin Guangfeng, Liu Weiguo, Xu Xin, Zhu Jialin, Zhao Shengmei, Qiu Taotao

机构信息

Physical Education and Health Guangxi Normal University Guilin China.

College of Sports and Health Guangxi College of Sports Education Nanning China.

出版信息

Food Sci Nutr. 2025 Sep 12;13(9):e70937. doi: 10.1002/fsn3.70937. eCollection 2025 Sep.

DOI:10.1002/fsn3.70937
PMID:40951591
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12431855/
Abstract

Exhaustive physical exercise, while promoting cardiovascular fitness, can paradoxically lead to excessive oxidative stress, systemic fatigue, and myocardial injury. Despite increasing awareness of exhaustion exercise myocardial damage, effective preventive strategies remain limited. Natural bioactive compounds with antioxidant and antiapoptotic properties have gained attention as potential interventions. Among them, triterpenoids derived from triterpenoids (GLTs) are notable for their potent free radical scavenging and cytoprotective effects. However, their cardioprotective potential under conditions of exhaustion exercise oxidative stress has not been fully elucidated. This study explores the antifatigue potential of GLTs and elucidates their underlying mechanisms through the establishment of a mouse model of exhaustion exercise via exhaustive treadmill running. This study showed that GLTs significantly alleviated exhaustion exercise by reducing serum fatigue biomarkers (CK, BUN, and LDH) and improving myocardial histopathological conditions. GLTs enhanced antioxidant capacity by decreasing MDA levels, increasing SOD and CAT activities, and elevating GSH content, thereby mitigating oxidative stress. Additionally, GLTs regulated apoptosis by downregulating Bax and Caspase-3 expression, upregulating Bcl-2 levels, and reducing the Bax/Bcl-2 ratio. Mechanistically, these effects were associated with activation of the Keap1/Nrf2/HO-1 signaling pathway. Collectively, this study provides new insights into the context-specific role of GLTs in protecting against exhaustion exercise myocardial injury. Our findings highlight the therapeutic potential of GLTs as a natural antioxidant strategy for mitigating oxidative stress, delaying fatigue, and preserving cardiac function under conditions of intensive physical exertion.

摘要

力竭性体育锻炼虽然能促进心血管健康,但自相矛盾的是,它会导致过度的氧化应激、全身疲劳和心肌损伤。尽管人们对力竭运动导致的心肌损伤的认识不断提高,但有效的预防策略仍然有限。具有抗氧化和抗凋亡特性的天然生物活性化合物作为潜在的干预措施受到了关注。其中,源自三萜类化合物(GLTs)的三萜因其强大的自由基清除和细胞保护作用而值得注意。然而,它们在力竭运动氧化应激条件下的心脏保护潜力尚未得到充分阐明。本研究通过建立力竭跑步机跑步的小鼠力竭运动模型,探讨了GLTs的抗疲劳潜力,并阐明其潜在机制。本研究表明,GLTs通过降低血清疲劳生物标志物(CK、BUN和LDH)和改善心肌组织病理学状况,显著减轻了力竭运动。GLTs通过降低MDA水平、增加SOD和CAT活性以及提高GSH含量来增强抗氧化能力,从而减轻氧化应激。此外,GLTs通过下调Bax和Caspase-3表达、上调Bcl-2水平以及降低Bax/Bcl-2比值来调节细胞凋亡。从机制上讲,这些作用与Keap1/Nrf2/HO-1信号通路的激活有关。总的来说,本研究为GLTs在预防力竭运动心肌损伤中的特定作用提供了新的见解。我们的研究结果突出了GLTs作为一种天然抗氧化策略的治疗潜力,可减轻氧化应激、延缓疲劳并在高强度体力消耗条件下保护心脏功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/032eb58266f4/FSN3-13-e70937-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/d475a9fdd09c/FSN3-13-e70937-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/1dc245a60d4e/FSN3-13-e70937-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/9dfff859887f/FSN3-13-e70937-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/110c7f5cf1ad/FSN3-13-e70937-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/aa825f9fdca2/FSN3-13-e70937-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/ad0d48da2311/FSN3-13-e70937-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/fae67f6dd259/FSN3-13-e70937-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/032eb58266f4/FSN3-13-e70937-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/d475a9fdd09c/FSN3-13-e70937-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/1dc245a60d4e/FSN3-13-e70937-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/9dfff859887f/FSN3-13-e70937-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/110c7f5cf1ad/FSN3-13-e70937-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/aa825f9fdca2/FSN3-13-e70937-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/ad0d48da2311/FSN3-13-e70937-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/fae67f6dd259/FSN3-13-e70937-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f834/12431855/032eb58266f4/FSN3-13-e70937-g003.jpg

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