Ishophloroglucin A, Isolated from Ishige okamurae, Alleviates Dexamethasone-Induced Muscle Atrophy through Muscle Protein Metabolism In Vivoopen access
- Authors
- Yang, Hye-Won; Oh, Seyeon; Chung, Dong-Min; Seo, Minyoung; Park, Shin Jae; Jeon, You-Jin; Byun, Kyunghee; Ryu, BoMi
- Issue Date
- May-2022
- Publisher
- MDPI
- Keywords
- Ishige okamurae; Ishophloroglucin A; muscle atrophy; muscle growth; muscle protein metabolism
- Citation
- Marine Drugs, v.20, no.5
- Journal Title
- Marine Drugs
- Volume
- 20
- Number
- 5
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/84553
- DOI
- 10.3390/md20050280
- ISSN
- 1660-3397
- Abstract
- The in vitro capacity of Ishige okamurae extract (IO) to improve impaired muscle function has been previously examined. However, the mechanism underlying IO-mediated muscle protein metabolism and the role of its component, Ishophloroglucin A (IPA), in mice with dexamethasone (Dexa)-induced muscle atrophy remains unknown. In the present study, we evaluated the effect of IO and IPA supplementation on Dexa-induced muscle atrophy by assessing muscle protein metabolism in gastrocnemius and soleus muscles of mice. IO and IPA supplementation improved the Dexa-induced decrease in muscle weight and width, leading to enhanced grip strength. In addition, IO and IPA supplementation regulated impaired protein synthesis (PI3K and Akt) or degradation (muscle-specific ubiquitin ligase muscle RING finger and atrogin-1) by modulating mRNA levels in gastrocnemius and soleus muscles. Additionally, IO and IPA upregulated mRNA levels associated with muscle growth activation (transient receptor potential vanilloid type 4 and adenosine A1 receptor) or inhibition (myostatin and sirtuin 1) in gastrocnemius and soleus muscle tissues of Dexa-induced mice. Collectively, these results suggest that IO and IO-derived IPA can regulate muscle growth through muscle protein metabolism in Dexa-induced muscle atrophy. © 2022 by the authors. Licensee MDPI, Basel, Switzerland.
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