ArticleHistochemistry and cell biology2012
Quantitative evaluation of the beneficial effects in the mdx mouse of epigallocatechin gallate, an antioxidant polyphenol from green tea.
Article in Histochemistry and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
30 citing papers in PubMed.
- Epigenetic modulation of the gut-muscle axis in pompe disease: Microbiota fingerprints to cellular and molecular pathomechanisms.Molecular metabolism · 2026Review
- Repurposed Nrf2 activator dimethyl fumarate rescues muscle inflammation and fibrosis in an aggravated mdx mouse model of Duchenne muscular dystrophy.Redox biology · 2025Article
- Decoding Neuromuscular Disorders: The Complex Role of Genetic and Epigenetic Regulators.Genes · 2025Review
- Cilostazol attenuates oxidative stress and apoptosis in the quadriceps muscle of the dystrophic mouse experimental model.International journal of experimental pathology · 2023Article
- The Role of Oxidative Stress in Skeletal Muscle Myogenesis and Muscle Disease.Antioxidants (Basel, Switzerland) · 2022Review
- FoxP1 is a transcriptional repressor associated with cancer cachexia that induces skeletal muscle wasting and weakness.Journal of cachexia, sarcopenia and muscle · 2021Article
- Nutraceutical Screening in a Zebrafish Model of Muscular Dystrophy: Gingerol as a Possible Food Aid.Nutrients · 2021Article
- Safety issues and harmful pharmacological interactions of nutritional supplements in Duchenne muscular dystrophy: considerations for Standard of Care and emerging virus outbreaks.Pharmacological research · 2020Review
- Therapeutic developments for Duchenne muscular dystrophy.Nature reviews. Neurology · 2019Review
- Article
- Molecular hydrogen alleviates motor deficits and muscle degeneration in mdx mice.Redox report : communications in free radical research · 2017Article
- Nutraceuticals and Their Potential to Treat Duchenne Muscular Dystrophy: Separating the Credible from the Conjecture.Nutrients · 2016Review
- The high correlation between counts and area fractions of lipofuscin granules, a biomarker of oxidative stress in muscular dystrophies.Histochemistry and cell biology · 2016Article
- Oxidative Stress-Mediated Skeletal Muscle Degeneration: Molecules, Mechanisms, and Therapies.Oxidative medicine and cellular longevity · 2016Review
- Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Physiological reviews · 2016Review
- Pharmacological therapeutics targeting the secondary defects and downstream pathology of Duchenne muscular dystrophy.Expert opinion on orphan drugs · 2016Article
- The role of oxidative stress in skeletal muscle injury and regeneration: focus on antioxidant enzymes.Journal of muscle research and cell motility · 2015Review
- Green tea component EGCG, insulin and IGF-1 promote nuclear efflux of atrophy-associated transcription factor Foxo1 in skeletal muscle fibers.The Journal of nutritional biochemistry · 2015Article
- Metabogenic and Nutriceutical Approaches to Address Energy Dysregulation and Skeletal Muscle Wasting in Duchenne Muscular Dystrophy.Nutrients · 2015Review
- What has the mdx mouse model of Duchenne muscular dystrophy contributed to our understanding of this disease?Journal of muscle research and cell motility · 2015Review
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In two separate previous studies, we reported that subcutaneous (sc) or oral administration of (-)-epigallocatechin-3-gallate (EGCG) limited the development of muscle degeneration of mdx mice, a mild phenotype model for Duchenne muscular dystrophy (DMD). However, it was not possible to conclude which was the more efficient route of EGCG administration because different strains of mdx mice, periods of treatment and methods of assessment were used. In this study, we investigated which administration routes and dosages of EGCG are the most effective for limiting the onset of dystrophic lesions in the same strain of mdx mice and applying the same methods of assessment. Three-week-old mdx mice were injected sc for 5 weeks with either saline or a daily average of 3 or 6 mg/kg EGCG. For comparison, age-matched mdx mice were fed for 5 weeks with either a diet containing 0.1% EGCG or a control diet. The effects of EGCG were assessed quantitatively by determining the activities of serum muscle-derived creatine kinase, isometric contractions of triceps surae muscles, integrated spontaneous locomotor activities, and oxidative stress and fibrosis in selected muscles. Oral administration of 180 mg/kg/day EGCG in the diet was found the most effective for significantly improving several parameters associated with muscular dystrophy. However, the improvements were slightly less than those observed previously for sc injection started immediately after birth. The efficacy of EGCG for limiting the development of dystrophic muscle lesions in mice suggests that EGCG may be of benefit for DMD patients.
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