| Autor: |
Rahman MM; Department of Nutritional Physiology, Institute of Medical Nutrition, Tokushima University Graduate School., Ulla A; Department of Nutritional Physiology, Institute of Medical Nutrition, Tokushima University Graduate School., Moriwaki H; Hamari Chemicals Ltd., Yasukawa Y; Hamari Nutritional Sciences Ltd., Uchida T; Department of Nutritional Physiology, Institute of Medical Nutrition, Tokushima University Graduate School., Nikawa T; Department of Nutritional Physiology, Institute of Medical Nutrition, Tokushima University Graduate School. |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of nutritional science and vitaminology [J Nutr Sci Vitaminol (Tokyo)] 2024; Vol. 70 (3), pp. 219-227. |
| DOI: |
10.3177/jnsv.70.219 |
| Abstrakt: |
This study investigated the protective effect of carnosine and its components (L-histidine and β-alanine [HA]) against dexamethasone (Dex)-induced muscle atrophy in C2C12 myotubes. Myotubes were treated with Dex (10 μM) to induce muscle atrophy manifested by decreased myotube diameter, low myosin heavy chain content, and increased expression of muscle atrophy-associated ubiquitin ligases (Atrogin-1, MuRF-1, and Cbl-b). Carnosine (20 mM) treatment significantly improved the myotube diameter and MyHC protein expression level in Dex-treated C2C12 myotubes. It also downregulated the expression of Atrogin-1, MuRF-1, and Cbl-b and suppressed the expression of forkhead box O3 (FoxO3a) mediated by Dex. Furthermore, reactive oxygen species production was increased by Dex but was ameliorated by carnosine treatment. However, HA (20 mM), the component of carnosine, treatment was found ineffective in preventing Dex-induced protein damage. Therefore, based on above results it can be suggested that carnosine could be a potential therapeutic agent to prevent Dex-induced muscle atrophy compared to its components HA. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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