Murata Motoki, Takahashi Rina, Marugame Yuki, Fujimura Yoshinori, Tachibana Hirofumi
Advanced Research Support Center (ADRES), Ehime University, Matsuyama, Ehime, Japan.
Graduate School of Agriculture, Ehime University, Matsuyama, Ehime, Japan.
Biochem Biophys Rep. 2024 Nov 23;40:101884. doi: 10.1016/j.bbrep.2024.101884. eCollection 2024 Dec.
Delphinidin, a plant anthocyanidin, suppresses disuse muscle atrophy in mice. However, its effect on muscle fiber type shift is unclear. To examine whether delphinidin affects skeletal muscle fiber type, differentiated C2C12 cells were treated with delphinidin. Results revealed that delphinidin upregulated the mRNA expression of myosin heavy chain type I (MyHCI), troponin C1, troponin I1, and MyHCIIx and increased slow MyHC protein level in C2C12 myotubes. Delphinidin also enhanced succinic dehydrogenase (SDH) activities and suppressed lactate dehydrogenase (LDH) activity. Adenosine monophosphate-activated protein kinase (AMPK) inhibition attenuated delphinidin-induced MyHCI upregulation and MyHCIIb downregulation. We investigated the effect of delphinidin on the upstream factors involved in AMPK activation. Delphinidin increased liver kinase B1 (LKB1) phosphorylation and nuclear respiratory factor 1 (NRF1) and calcium/calmodulin-dependent protein kinase 2 (CaMKK2) protein levels. In conclusion, delphinidin induced muscle fiber type conversion from fast-twitch to slow-twitch muscles through the AMPK signaling pathway.
飞燕草素是一种植物花青素，可抑制小鼠的废用性肌肉萎缩。然而，其对肌纤维类型转变的影响尚不清楚。为了研究飞燕草素是否影响骨骼肌纤维类型，用飞燕草素处理分化的C2C12细胞。结果显示，飞燕草素上调了I型肌球蛋白重链（MyHCI）、肌钙蛋白C1、肌钙蛋白I1和MyHCIIx的mRNA表达，并增加了C2C12肌管中慢肌球蛋白重链蛋白水平。飞燕草素还增强了琥珀酸脱氢酶（SDH）活性并抑制了乳酸脱氢酶（LDH）活性。单磷酸腺苷激活蛋白激酶（AMPK）抑制减弱了飞燕草素诱导的MyHCI上调和MyHCIIb下调。我们研究了飞燕草素对参与AMPK激活的上游因子的影响。飞燕草素增加了肝激酶B1（LKB1）的磷酸化以及核呼吸因子1（NRF1）和钙/钙调蛋白依赖性蛋白激酶2（CaMKK2）的蛋白水平。总之，飞燕草素通过AMPK信号通路诱导肌纤维类型从快肌向慢肌转变。
