ArticleFrontiers in pharmacology2022
Trilobatin, a Naturally Occurring Food Additive, Ameliorates Exhaustive Exercise-Induced Fatigue in Mice: Involvement of Nrf2/ARE/Ferroptosis Signaling Pathway.
Article in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- Nutritional Interventions and Acupuncture-Based Strategies for Exercise-Induced Fatigue and Recovery: Mechanisms and Integrative Perspectives.Food science & nutrition · 2026Review
- Study on the Anti-fatigue Effects of Polysaccharides from Erjing Formula.Current pharmaceutical biotechnology · 2026Article
- Adhesive-Electrocoupling Hydrogels for Tissue Regeneration: Design, Mechanisms, and Perspectives.Research (Washington, D.C.) · 2026Review
- Irisin prevents liver injury during exhausting physical activity by suppressing ferroptosis via Nrf2/GPX4 signaling.BMC gastroenterology · 2025Article
- Trilobatin, a Naturally Occurring GPR158 Ligand, Alleviates Depressive-like Behavior by Promoting Mitophagy.Journal of agricultural and food chemistry · 2025Article
- Gallic acid alleviates exercise-induced muscle damage by inhibiting mitochondrial oxidative stress and ferroptosis.Journal of translational medicine · 2025Article
- Ethanol extract of propolis relieves exercise-induced fatigue via modulating the metabolites and gut microbiota in mice.Frontiers in nutrition · 2025Article
- Peroxisomal homeostasis in metabolic diseases and its implication in ferroptosis.Cell communication and signaling : CCS · 2024Review
- Trilobatin contributes to the improvement of myopathy in a mouse model of Duchenne muscular dystrophy.International journal of experimental pathology · 2024Article
- Beyond Mortality: Exploring the Influence of Plant Phenolics on Modulating Ferroptosis-A Systematic Review.Antioxidants (Basel, Switzerland) · 2024Review
- Protective function of albiflorin against ferroptosis in exhaustive exerciseinduced myocardial injury via the AKT/Nrf2/HO-1 signaling.Acta cirurgica brasileira · 2024Article
- Signaling pathways regulated by natural active ingredients in the fight against exercise fatigue-a review.Frontiers in pharmacology · 2023Review
- Ferroptosis and its role in skeletal muscle diseases.Frontiers in molecular biosciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nrf2-mediated oxidative stress is a promising target of exhaustive exercise-induced fatigue (EEIF). Trilobatin (TLB) is a naturally occurring food additive with antioxidant effect and Nrf2 activation potency. The present study aimed to investigate the effect of TLB on EEIF and elucidate its underlying mechanism. Our results showed that TLB exerted potent anti-EEIF effect, as reflected by the rope climbing test and exhaustive swimming test. Moreover, TLB also effectively reduced the levels of lactate, creatine kinase, and blood urea nitrogen, and increased liver glycogen and skeletal muscle glycogen in mice after EEIF insult. Additionally, TLB also balanced the redox status as evidenced by decreasing the generation of reactive oxygen species and improving the antioxidant enzyme activities including superoxide dismutase, catalase, and glutathione peroxidase, as well as the level of glutathione both in the tissue of muscle and myocardium. Furthermore, TLB promoted nuclear factor erythroid 2-related factor 2 (Nrf2) from the cytoplasm to the nucleus, and upregulated its downstream antioxidant response element (ARE) including quinone oxidoreductase-1 and heme oxygenase-1. Intriguingly, TLB also upregulated the GPx4 protein expression and reduced iron overload in mice after EEIF insult. Encouragingly, the beneficial effect of TLB on EEIF-induced oxidative stress and ferroptosis were substantially abolished in Nrf2-deficient mice. In conclusion, our findings demonstrate, for the first time, that TLB alleviates EEIF-induced oxidative stress through mediating Nrf2/ARE/ferroptosis axis.
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