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Cited by 34Muscle Physiology and DisordersNeurogenetic and Muscular Disorders ResearchAmyotrophic Lateral Sclerosis Research

The Soy Isoflavone Genistein Blunts Nuclear Factor Kappa-B, MAPKs and TNF-α Activation and Ameliorates Muscle Function and Morphology in Mdx Mice

Messina, Sonia, Bitto, Alessandra, Aguennouz, M’hammed, Vita, Gian Luca, Polito, Francesca, Irrera, Natasha, Altavilla, Domenica, Marini, Herbert +3 more·2011·Neuromuscular Disorders
DOI 10.1016/j.nmd.2011.04.014
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Abstract

Several lines of evidence suggest a detrimental role of the nuclear factor-κB (NF-κB) activation in the dystrophic process. We showed in previous studies that its inhibition through drugs with antioxidant properties, have beneficial effects in mdx mice. We tested whether genistein, a well-known isoflavone, inhibitor of NF-κB, MAPK and TNF-α and readily available for clinical use, could have a beneficial effect in mdx mice in comparison with methylprednisolone, the gold standard treatment for DMD patients. Five-week old mdx mice received for five weeks: genistein (daily or 3-times/week), methylprednisolone or vehicle. Genistein treatment: (1) increased forelimb strength and strength normalized to weight; (2) reduced serum creatine-kinase levels; (3) reduced markers of oxidative stress; (4) reduced muscle necrosis and enhanced regeneration. The positive results were more evident with the daily administration of genistein and were comparable to the effect of corticosteroids. Our data support the novel hypothesis that, as other more specific therapeutic approaches are still under development, this soy-derived compound is a promising option to be further investigated in dystrophic process.

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Crossref · 10.1016/j.nmd.2011.04.014

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  • Intraperitoneal injections of genistein ameliorate muscle function and morphology in mdx mice through inhibiting oxidative stress and blunting proinflammatory factors, such as NF-κB, TNF-α, and MAPKs.

    “Intraperitoneal injections of genistein, a soy isoflavone, ameliorates muscle function and morphology in mdx mice through inhibiting oxidative stress and blunting proinflammatory factors, such as NF-κB, TNF-α, and MAPKs [114].”

    From Nutraceuticals in the Prevention and Treatment of the Muscle Atrophy (2021) · cites this paper as [114]

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Authors
Messina, S., Bitto, A., Aguennouz, M., Vita, G. L., Polito, F., Irrera, N., Altavilla, D., Marini, H., Migliorato, A., Squadrito, F., & Vita, G.
Affiliations
University of Messina (IT)
Corresponding author
Messina, Sonia
ORCID
Venue
Neuromuscular Disorders
Publisher
Elsevier BV
Published
2011-08
Volume
21
Issue
8
Pages
579-589
ISSN
0960-8966 (ISSN-L)
DOI
10.1016/j.nmd.2011.04.014
OpenAlex
W2161743223
Cited by
33
References
55
Citations by year
2025: 1 · 2023: 1 · 2022: 1 · 2021: 5 · 2020: 2 · 2019: 4 · 2018: 2 · 2017: 2 · 2016: 2 · 2015: 7 · 2014: 1 · 2013: 2 · 2012: 3
FWCI
0.78
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Neuromuscular Disorders (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institutes of Health
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Genetics › Neurogenetic and Muscular Disorders Research
  • Health Sciences › Medicine › Neurology › Amyotrophic Lateral Sclerosis Research
Keywords
genistein, isoflavones, mdx mice, Duchenne muscular dystrophy, NF-κB, mitogen-activated protein kinase, TNF-α, methylprednisolone, muscle strength, creatine kinase, oxidative stress, muscle regeneration, muscle necrosis, antioxidant therapy
MeSH terms
Animals, Creatine Kinase, Disease Models, Animal, Glucocorticoids, Male, Methylprednisolone, Mice, Inbred C57BL, Regeneration, Tumor Necrosis Factor-alpha, Signal Transduction, NF-kappa B, Mice, Inbred mdx, Oxidative Stress, Muscle, Skeletal, Genistein, Muscular Dystrophy, Duchenne, Mitogen-Activated Protein Kinase Kinases, Protein Kinase Inhibitors, Mice, Muscle Strength

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