Department of Molecular Orthopedics, Beijing Research Institute of Traumatology and Orthopedics, Beijing Jishuitan Hospital, Beijing 100035, P.R. China.
Department of Pediatric Cardiology, Heart Center, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, Guangdong 510623, P.R. China.
Mol Med Rep. 2021 Jul;24(1). doi: 10.3892/mmr.2021.12175. Epub 2021 Jun 3.
Diet and exercise are the most effective approaches used to induce weight loss. D‑psicose is a low‑calorie sweetener that has been shown to reduce weight in obese individuals. However, the effect of D‑psicose on muscle cells under oxidative stress, which is produced during exercise, requires further investigation. The present study aimed to determine the effects of D‑psicose on C2C12 myogenic cells in vitro. Hydrogen peroxide (HO) was used to stimulate the generation of intracellular reactive oxygen species (ROS) in muscle cells to mimic exercise conditions. Cell viability was analyzed using a MTT assay and flow cytometry was used to analyze the levels of apoptosis, mitochondrial membrane potential (MMP), the generation of ROS and the cell cycle distribution following treatment. Furthermore, protein expression levels were analyzed using western blotting and cell proliferation was determined using a colony formation assay. The results of the present study revealed that D‑psicose alone exerted no toxicity on C2C12 mouse myogenic cells. However, in the presence of low‑dose (100 M) HO‑induced ROS, D‑psicose induced C2C12 cell injury and significantly decreased C2C12 cell viability in a dose‑dependent manner. In addition, the levels of apoptosis and the generation of ROS increased, while the MMP decreased. MAPK family molecules were also activated in a dose‑dependent manner following treatment. Notably, the combined treatment induced G/M phase arrest and reduced the proliferation of C2C12 cells. In conclusion, the findings of the present study suggested that D‑psicose may induce toxic effects on muscle cells in a simulated exercise situation by increasing ROS levels, activating the MAPK signaling pathway and disrupting the MMP.
饮食和运动是诱导体重减轻最有效的方法。D-阿洛酮糖是一种低热量甜味剂，已被证明可减轻肥胖个体的体重。然而，在运动过程中产生的氧化应激下，D-阿洛酮糖对肌肉细胞的影响仍需要进一步研究。本研究旨在确定 D-阿洛酮糖对 C2C12 成肌细胞的体外影响。过氧化氢（H2O2）用于刺激肌肉细胞内活性氧（ROS）的产生，以模拟运动条件。使用 MTT 测定法分析细胞活力，并用流式细胞术分析细胞凋亡、线粒体膜电位（MMP）、ROS 生成和细胞周期分布的水平。此外，还使用 Western blot 分析蛋白表达水平，并使用集落形成测定法测定细胞增殖。本研究结果表明，D-阿洛酮糖单独作用于 C2C12 小鼠成肌细胞时没有毒性。然而，在低剂量（100 μM）H2O2 诱导的 ROS 存在下，D-阿洛酮糖诱导 C2C12 细胞损伤，并以剂量依赖性方式显著降低 C2C12 细胞活力。此外，细胞凋亡水平和 ROS 生成增加，而 MMP 降低。MAPK 家族分子也被激活。值得注意的是，联合处理诱导 G/M 期停滞并减少 C2C12 细胞的增殖。综上所述，本研究结果表明，D-阿洛酮糖可能通过增加 ROS 水平、激活 MAPK 信号通路和破坏 MMP 对模拟运动条件下的肌肉细胞产生毒性作用。
