Journal
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
Volume 65, Issue 1, Pages 45-50Publisher
AMER CHEMICAL SOC
DOI: 10.1021/acs.jafc.6b03661
Keywords
delphinidin; muscle atrophy; ubiquitin ligase; microRNA; NFATc3
Funding
- Japan Society for the Promotion of Science [15H02448]
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Delphinidin, one of the major anthocyanidins, shows protective effects against a variety of pathologies, including cancer, inflammation, and muscle atrophy. The purpose of this study was to determine the preventive mechanism of delphinidin on disuse muscle atrophy. In vitro and in vivo models were used to validate the effects of delphinidin on the expression of MuRF1, miR-23a, and NFATc3. Delphinidin suppressed the upregulation of MuRF1 (1.77 +/- 0.05 vs 1.03 +/- 0.17, P < 0.05) expression and inhibited the downregulation of miR-23a (0.56 +/- 0.05 vs 0.94 +/- 0.06, P < 0.05) and NFATc3 (0.61 +/- 0.02 vs 1.02 +/- 0.08, P < 0.01) expression in dexamethasone-treated C2C12 cells. In gastrocnemius, muscle weight loss was prevented by oral administration of delphinidin. Moreover, delphinidin suppressed MuRF1 (3.35 +/- 0.13 vs 2.26 +/- 0.3, P < 0.01) expression and promoted miR-23a (0.58 +/- 0.15 vs 2.25 +/- 0.29, P < 0.001) and NFATc3 (0.85 +/- 0.17 vs 1.54 +/- 0.13, P < 0.001) expressions. Delphinidin intake may prevent disuse muscle atrophy by inducing miR-23a expression and suppressing MuRF1 expression.
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