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Delphinidin Prevents Muscle Atrophy and Upregulates miR-23a Expression.

Abstract
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.
AuthorsMotoki Murata, Haruna Nonaka, Satomi Komatsu, Megumi Goto, Mai Morozumi, Shuhei Yamada, I-Chian Lin, Shuya Yamashita, Hirofumi Tachibana
JournalJournal of agricultural and food chemistry (J Agric Food Chem) Vol. 65 Issue 1 Pg. 45-50 (Jan 11 2017) ISSN: 1520-5118 [Electronic] United States
PMID28000445 (Publication Type: Journal Article)
Chemical References
  • Anthocyanins
  • Glucocorticoids
  • MicroRNAs
  • Mirn23b microRNA, mouse
  • Muscle Proteins
  • NFATC Transcription Factors
  • Nfatc3 protein, mouse
  • Tripartite Motif Proteins
  • Trim63 protein, mouse
  • Ubiquitin-Protein Ligases
  • delphinidin
Topics
  • Animals
  • Anthocyanins (administration & dosage)
  • Glucocorticoids (adverse effects)
  • Humans
  • Male
  • Mice
  • Mice, Inbred C57BL
  • MicroRNAs (genetics, metabolism)
  • Muscle Proteins (genetics, metabolism)
  • Muscle, Skeletal (drug effects, metabolism)
  • Muscular Atrophy (drug therapy, genetics, metabolism)
  • NFATC Transcription Factors (genetics, metabolism)
  • Tripartite Motif Proteins (genetics, metabolism)
  • Ubiquitin-Protein Ligases (genetics, metabolism)
  • Up-Regulation (drug effects)

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