| Literature DB >> 28000445 |
Motoki Murata1, Haruna Nonaka1, Satomi Komatsu1, Megumi Goto1, Mai Morozumi1, Shuhei Yamada1, I-Chian Lin1, Shuya Yamashita1, Hirofumi Tachibana1.
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.Entities:
Keywords: NFATc3; delphinidin; microRNA; muscle atrophy; ubiquitin ligase
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Year: 2016 PMID: 28000445 DOI: 10.1021/acs.jafc.6b03661
Source DB: PubMed Journal: J Agric Food Chem ISSN: 0021-8561 Impact factor: 5.279