Astragalus polysaccharide attenuates overexercise-induce myocardial injury via activating AMPK signaling pathway to suppress inflammation and oxidative stress

Tuo, Xinling; Deng, Zuhu; Huang, Guochao; Gong, Huiping; Xie, Hui

doi:10.1590/0001-3765202120210314

Cited by 6 publications

(7 citation statements)

References 22 publications

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“…Furthermore, nuclear factor kappa B (NF-κB), as a transcription factor that activates the release of pro-inflammatory cytokines and generate a vicious circle of inflammatory response and mitochondrial dysfunction, as well as impaired mitochondria, produces large amounts of ROS, resulting in decreased muscle strength and fatigue [ 39 , 43 ]. Interestingly, astragalus polysaccharide (APS) has a protective effect on myocardial injury induced by excessive exercise in SD rat by activating the AMPK pathway, constricting the production of ROS, and reducing the levels of IL-1β, TNF-α, and NF-κB [ 98 ]. Additionally, interleukin-8 (IL-8) is also involved in mediating the development of inflammation.…”

Section: Polysaccharides Ameliorate Fatiguementioning

confidence: 99%

“…Known as important regulators of cellular metabolic homeostasis, the AMPK and PGC-1α pathways play a key role in autophagy activity, inflammation reaction, and insulin resistance in skeletal muscle tissues [ 83 , 84 ]. Some polysaccharides also effectively activated the AMPK and PGC-1α pathway, which suppress inflammation and oxidative stress to achieve anti-fatigue effects [ 68 , 78 , 98 ]. However, the relationship between polysaccharides and the gut-muscle axis remains unclear and requires further investigation.…”

Section: Polysaccharides Ameliorate Fatigue Via the Gut-muscle Axismentioning

confidence: 99%

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Dietary Polysaccharides Exert Anti-Fatigue Functions via the Gut-Muscle Axis: Advances and Prospectives

Zhou,

Chu,

Luo

et al. 2023

Foods

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Due to today’s fast-paced lifestyle, most people are in a state of sub-health and face “unexplained fatigue”, which can seriously affect their health, work efficiency, and quality of life. Fatigue is also a common symptom of several serious diseases such as Parkinson’s, Alzheimer’s, cancer, etc. However, the contributing mechanisms are not clear, and there are currently no official recommendations for the treatment of fatigue. Some dietary polysaccharides are often used as health care supplements; these have been reported to have specific anti-fatigue effects, with minor side effects and rich pharmacological activities. Dietary polysaccharides can be activated during food processing or during gastrointestinal transit, exerting unique effects. This review aims to comprehensively summarize and evaluate the latest advances in the biological processes of exercise-induced fatigue, to understand dietary polysaccharides and their possible molecular mechanisms in alleviating exercise-induced fatigue, and to systematically elaborate the roles of gut microbiota and the gut-muscle axis in this process. From the perspective of the gut-muscle axis, investigating the relationship between polysaccharides and fatigue will enhance our understanding of fatigue and may lead to a significant breakthrough regarding the molecular mechanism of fatigue. This paper will provide new perspectives for further research into the use of polysaccharides in food science and food nutrition, which could help develop potential anti-fatigue agents and open up novel therapies for sub-health conditions.

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Section: Polysaccharides Ameliorate Fatiguementioning

confidence: 99%

Section: Polysaccharides Ameliorate Fatigue Via the Gut-muscle Axismentioning

confidence: 99%

Dietary Polysaccharides Exert Anti-Fatigue Functions via the Gut-Muscle Axis: Advances and Prospectives

Zhou,

Chu,

Luo

et al. 2023

Foods

View full text Add to dashboard Cite

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“…Long-term exercise-induced fatigue causes myocardial cell apoptosis, which leads to abnormal morphological structure of myocardial cell nucleus and increased apoptosis rate. Excessive apoptosis of myocardial cells affects the overall heart structure and function, and even causes sudden cardiac death (45). Tuo et al (46) evaluated the changes of myocardial morphology, injury indexes, and inflammatory-related proteins in overtraining rats, and found that astragalus polysaccharides significantly increased the cell viability of H9c2 cells, reduced the apoptosis of myocardial cells, and reduced myocardial injury related indicators.…”

Section: Cardiac Phenotypementioning

confidence: 99%

Establishment and identification of an animal model of long-term exercise-induced fatigue

et al. 2022

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In competitive sports, the training load is close to the human physiological limit, which will inevitably lead to exercise-induced fatigue. If fatigue cannot be recovered in time, it will eventually lead to excessive training and affect sport performance. Therefore, fatigue has become an important part of the physical function assessment for athletes. This paper will review animal models of long-term exercise-induced fatigue, modeling schemes of mice under treadmill and swimming training, phenotypes of long-term exercise-induced fatigue (e.g., nervous system damage, myocardial cell damage, bone mineral density changes, and skeletal muscle damage), and fatigue indicators. The relationship between physiological indicators and biomarkers and long-term exercise-induced fatigue is analyzed to promote exercise-induced fatigue monitoring. This paper attempts to provide a reference for the selection of animal models of long-term exercise-induced fatigue and provide a new theoretical basis for medical supervision and recovery of exercise-induced fatigue.

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“…To a large extent, APS has regulatory effects on the immune functions of the human body 9 . APS also shows anti‐viral, anti‐tumour, anti‐aging, anti‐stress and anti‐oxidation effects in the development of different diseases 10–12 . Importantly, APS was demonstrated to ameliorate cisplatin‐induced acute kidney injury (AKI) by inhibiting oxidative damage and mitochondrial dysfunction 13 and exert a protective effect in sepsis‐induced AKI 14 .…”

Section: Introductionmentioning

confidence: 99%

Astragalus polysaccharide alleviates angiotensin II‐induced glomerular podocyte dysfunction by inhibiting the expression of RARRES1 and LCN2

Peng

Zhang

Xiao

2023

Clin Exp Pharma Physio

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Podocyte loss is a predictor of kidney disease development, including diabetic nephropathy. Astragalus polysaccharide (APS) was considered a renoprotective drug, whereas the mechanisms operated by APS on podocyte dysfunction are rarely mentioned. This study aims at the mechanistic underlying of APS on angiotensin II (Ang II)-induced podocyte dysfunction. Mouse glomerular podocytes MPC5 were induced with Ang II, the morphologic changes were observed and nephrin, desmin and Wilms' tumour protein-1 (WT-1) levels were determined. The MPC5 cells were treated with APS (50, 100 and 200 μg/mL) and transduced with retinoic acid receptor responder protein 1 (RARRES1) overexpression vectors. The expression of RARRES1, lipocalin-2 (LCN2), nephrin and desmin was tested, MPC5 cell viability and apoptosis were evaluated, and the levels of an endocytotic receptor megalin, Bcl-2, Bax, interleukin (IL)-6, IL-1β and tumour necrosis factor (TNF)-α were assessed. The binding of RARRES1 to LCN2 was predicted and verified. Mice were infused with Ang II to evaluate histopathological alterations and 24-h urinary albumin content. Ang II induction suppressed MPC5 cell viability, reduced the expression of nephrin, WT-1, megalin

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Astragalus polysaccharide attenuates overexercise-induce myocardial injury via activating AMPK signaling pathway to suppress inflammation and oxidative stress

Cited by 6 publications

References 22 publications

Dietary Polysaccharides Exert Anti-Fatigue Functions via the Gut-Muscle Axis: Advances and Prospectives

Dietary Polysaccharides Exert Anti-Fatigue Functions via the Gut-Muscle Axis: Advances and Prospectives

Establishment and identification of an animal model of long-term exercise-induced fatigue

Astragalus polysaccharide alleviates angiotensin II‐induced glomerular podocyte dysfunction by inhibiting the expression of RARRES1 and LCN2

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