Murata Motoki, Nonaka Haruna, Komatsu Satomi, Goto Megumi, Morozumi Mai, Yamada Shuhei, Lin I-Chian, Yamashita Shuya, Tachibana Hirofumi
Division of Applied Biological Chemistry, Department of Bioscience and Biotechnology, Faculty of Agriculture, Kyushu University , Fukuoka 812-8581, Japan.
J Agric Food Chem. 2017 Jan 11;65(1):45-50. doi: 10.1021/acs.jafc.6b03661. Epub 2016 Dec 29.
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.
矢车菊素是主要的花青素之一,对包括癌症、炎症和肌肉萎缩在内的多种病症具有保护作用。本研究的目的是确定矢车菊素对废用性肌肉萎缩的预防机制。采用体外和体内模型来验证矢车菊素对肌肉萎缩相关基因1(MuRF1)、微小RNA-23a(miR-23a)和活化T细胞核因子3(NFATc3)表达的影响。矢车菊素抑制了地塞米松处理的C2C12细胞中MuRF1表达的上调(1.77±0.05对1.03±0.17,P<0.05),并抑制了miR-23a(0.56±0.05对0.94±0.06,P<0.05)和NFATc3(0.61±0.02对1.02±0.08,P<0.01)表达的下调。在腓肠肌中,口服矢车菊素可防止肌肉重量减轻。此外,矢车菊素抑制了MuRF1(3.35±0.13对2.26±0.3,P<0.01)的表达,并促进了miR-23a(0.58±0.15对2.25±0.29,P<0.001)和NFATc3(0.85±0.17对1.54±0.13,P<0.001)的表达。摄入矢车菊素可能通过诱导miR-23a表达和抑制MuRF1表达来预防废用性肌肉萎缩。