Abstract:Abstract: Mouse C3H muscle myoblast (C2C12) was used as the cell model to investigate the effects of low glucose stress on myoblast proliferation and its underlying mechanism by measuring cell proliferation, cell cycle, adenosine triphosphate (ATP) level, reactive oxygen species (ROS) generation, mitochondrial membrane potential (MMP) and expression of sirtuin1 (SIRT1). C2C12 myoblasts proliferation (P<0.01) was inhibited by low glucose stress (LG, 5 mmol/L) compared with the control group (22.5 mmol/L) on the third day. The cells were markedly arrested at the G0/G1 phase (P<0.05). The DCF fluorescence intensity (P<0.05) (the quantity of ROS generation) and MMP (P<0.05) in the C2C12 myoblasts of the LG group significantly decreased, but SIRT1, FOXO3a (forkhead box O3a), p27 (p27/Kip1) mRNA expression and the ATP activity in the C2C12 myoblasts of the LG group significantly increased (P<0.05). It could be concluded that the expression of SIRT1/FOXO3a/p27 mRNA were increased by low glucose stress in C2C12 myoblast, which can contribute to the inhibition of cell proliferation and arresting in cell cycle. What′s more, the mitochondrial energy metabolism efficiency of C2C12 myoblasts would also be enhanced by low glucose stress.
引用本文:
李方晖, 徐呈祥, 冯庆鲲. 低糖应激对成肌细胞增殖的影响及其机制[J]. 生命科学研究, 2016, 20(1): 29-35.
LI Fang-Hui, XU Cheng-Xiang, FENG Qing-Kun. Effect of Low Glucose Stress on Proliferation of C2C12 Myoblast and Its Mechanism. Life Science Research, 2016, 20(1): 29-35.