Sulforaphane treatment protects skeletal muscle against damage induced by exhaustive exercise in rats
Abstract
Sulforaphane (SF), one of the most important isothiocyanates in the human diet, present in cruciferous vegetables, is known to have chemopreventive activities in different tissues. No data are available on its effects in the prevention of skeletal muscle damage. In this study, we investigated the potential protective effects of SF treatment on muscle damage and oxidative stress induced by an acute bout of exhaustive exercise in rats. Male Wistar rats were treated with SF (25 mg/kg body wt ip) for 3 days before undergoing an acute exhaustive exercise protocol in a treadmill (+7% slope and 24 m/min). Acute exercise resulted in a significant increase in plasma lactate dehydrogenase (LDH) and creatine phosphokinase (CPK) activities. It also resulted in a significant increase in thiobarbituric acid-reactive substances, in a significant decrease in tissue total antioxidant capacity, and in a significant decrease in NAD(P)H:quinone oxidoreductase 1 (NQO1) expression and activity in vastus lateralis muscle. SF treatment significantly increased muscle NQO1, glutathione- S-transferase, and glutathione reductase expression and activity, with no effect on glutathione peroxidase and thioredoxin reductase. The observed SF-induced upregulation of phase II enzymes was accompanied by a significant increase in nuclear erythroid 2 p45-related factor 2 expression and correlated with a significant increase in total antioxidant capacity and a decrease in plasma LDH and CPK activities. Our data demonstrate that SF acts as an indirect antioxidant in skeletal muscle and could play a critical role in the modulation of the muscle redox environment, leading to the prevention of exhaustive exercise-induced muscle damage.
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Treatment of rodents with sulforaphane can increase endurance capacity via the NFE2L2-ARE pathway.
“previous studies have shown that treatment of rodents with sulforaphane can increase endurance capacity via the NFE2L2-ARE pathway (32, 33).”
From Skeletal muscle NOX4 is required for adaptive responses that prevent insulin resistance (2021) · cites this paper as [33]
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- Authors
- Malaguti, M., Angeloni, C., Garatachea, N., Baldini, M., Leoncini, E., Collado, P. S., Teti, G., Falconi, M., Gonzalez-Gallego, J., & Hrelia, S.
- Affiliations
- University of Bologna (IT)
- Universidad de León (ES)
- Institute of Biomedicine, University of León, León, Spain; and
- Corresponding author
- Hrelia, Silvana
- ORCID
- Venue
- Journal of Applied Physiology
- Publisher
- American Physiological Society
- Published
- 2009-10
- Volume
- 107
- Issue
- 4
- Pages
- 1028-1036
- ISSN
- 0161-7567 (ISSN-L)
- 8750-7587
- 1522-1601
- OpenAlex
- W2171906474
- Cited by
- 103
- References
- 64
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 7 · 2023: 5 · 2022: 5 · 2021: 7 · 2020: 12 · 2019: 4 · 2018: 7 · 2017: 8 · 2016: 8 · 2015: 8 · 2014: 5 · 2013: 6 · 2012: 4
- FWCI
- 3.05
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Applied Physiology (publishedVersion)
- PubMed (publishedVersion)
- Archivio istituzionale della ricerca (Alma Mater Studiorum Università di Bologna) (submittedVersion)
- Unicam Scientific Publications (University of Camerino) (submittedVersion)
- Topics
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Keywords
- sulforaphane, isothiocyanates, skeletal muscle injury, exhaustive exercise, oxidative stress, NQO1, phase II enzymes, antioxidant capacity, Nrf2, glutathione S-transferase, glutathione reductase, creatine kinase, lactate dehydrogenase, chemoprevention
- MeSH terms
- Animals, Antioxidants, Creatine Kinase, Physical Exertion, Glutathione Peroxidase, Glutathione Reductase, Glutathione Transferase, L-Lactate Dehydrogenase, Male, Muscular Diseases, Oxidation-Reduction, Sulfoxides, Thiocyanates, Thioredoxin-Disulfide Reductase, NAD(P)H Dehydrogenase (Quinone), Rats, Wistar, Thiobarbituric Acid Reactive Substances, Isothiocyanates, Oxidative Stress, NF-E2-Related Factor 2, Rats, Quadriceps Muscle
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