Cited by 34Muscle Physiology and DisordersBioactive natural compoundsMuscle metabolism and nutrition

Corylifol A from Psoralea corylifolia L. Enhances Myogenesis and Alleviates Muscle Atrophy

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Han, Yeongeun, Lee, Hyejin, Li, Hua, Ryu, Jae-Ha·2020·International Journal of Molecular Sciences

Abstract

Inflammatory conditions caused by cancer, chronic diseases or aging can lead to skeletal muscle atrophy. We identified myogenic compounds from Psoralea corylifolia (PC), a medicinal plant that has been used for the treatment of inflammatory and skin diseases. C2C12 mouse skeletal myoblasts were differentiated in the presence of eight compounds isolated from PC to evaluate their myogenic potential. Among them, corylifol A showed the strongest transactivation of MyoD and increased expression of myogenic markers, such as MyoD, myogenin and myosin heavy chain (MHC). Corylifol A increased the number of multinucleated and MHC-expressing myotubes. We also found that the p38 MAPK signaling pathway is essential for the myogenic action of corylifol A. Atrophic condition was induced by treatment with dexamethasone. Corylifol A protected against dexamethasone-induced myotube loss by increasing the proportion of multinucleated MHC-expressing myotubes compared with dexamethasone-damaged myotubes. Corylifol A reduced the expression of muscle-specific ubiquitin-E3 ligases (MAFbx and MuRF1) and myostatin, while activating Akt. These dual effects of corylifol A, inhibition of catabolic and activation of anabolic pathways, protect myotubes against dexamethasone damage. In summary, corylifol A isolated from P. corylifolia alleviates muscle atrophic condition through activating myoblast differentiation and suppressing muscle degradation in atrophic conditions.

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Crossref · 10.3390/ijms21051571

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  • Corylifol A enhances myogenesis in C2C12 cells via the activation of p38 MAPKs.

    “Corylifol A, a phenolic compound from Psoralea corylifolia L., enhances myogenesis in C2C12 cells via the activation of p38 MAPKs.”
  • Corylifol A inhibits dexamethasone-induced muscle atrophy in C2C12 cells, related to inhibition of catabolic pathways and activation of the anabolic pathway.

    “It also inhibits dexamethasone-induced muscle atrophy in C2C12 cells, which is related to the inhibition of catabolic pathways and the activation of the anabolic pathway [101].”

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Authors
Han, Y., Lee, H., Li, H., & Ryu, J.-H.
Affiliations
  • Sookmyung Women's University (KR)
  • Research Institute of Pharmaceutical Sciences and College of Pharmacy, Sookmyung Women’s University, 100 Chungparo 47-Gil, Yongsan-Gu, Seoul 04310, Korea
Corresponding author
Ryu, Jae-Ha
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2020-02-25
Volume
21
Issue
5
Pages
1571
ISSN
1422-0067 (ISSN-L)
OpenAlex
W3006795980
Cited by
34
References
47
Citations by year
2026: 3 · 2025: 3 · 2024: 7 · 2023: 6 · 2022: 7 · 2021: 3 · 2020: 4 · 2019: 1
FWCI
1.62
Type
journal article
Language
en
Open access
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Sookmyung Women's University (1-201809-6)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bioactive natural compounds
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Muscle metabolism and nutrition
Keywords
Psoralea corylifolia, skeletal muscle atrophy, myogenesis, p38 MAPK signaling, dexamethasone-induced atrophy, atrogin-1, MuRF1, myostatin, Akt signaling, MyoD, myosin heavy chain, muscle degradation, medicinal plant constituents
MeSH terms
Tripartite Motif Proteins, Animals, Cell Line, Muscle Proteins, Muscular Atrophy, MyoD Protein, Muscle Fibers, Skeletal, Myosin Heavy Chains, Muscle Development, Ubiquitin-Protein Ligases, Flavones, p38 Mitogen-Activated Protein Kinases, Mice

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