Key Laboratory of Ruminant Molecular and Cellular Breeding, College of Animal Science and Technology, Ningxia University, Yinchuan 750021, China.
Animal Genomics and Improvement Laboratory, Henry A. Wallace Beltsville Agricultural Research Center, Agricultural Research Service, United States Department of Agriculture USDA, Beltsville, MD 20705, USA.
Int J Mol Sci. 2023 Aug 30;24(17):13474. doi: 10.3390/ijms241713474.
Sodium butyrate (NaB) is one of the short-chain fatty acids and is notably produced in large amounts from dietary fiber in the gut. Recent evidence suggests that NaB induces cell proliferation and apoptosis. Skeletal muscle is rich in plenty of mitochondrial. However, it is unclear how NaB acts on host muscle cells and whether it is involved in mitochondria-related functions in myocytes. The present study aimed to investigate the role of NaB treatment on the proliferation, apoptosis, and mitophagy of bovine skeletal muscle satellite cells (BSCs). The results showed that NaB inhibited proliferation, promoted apoptosis of BSCs, and promoted mitophagy in a time- and dose-dependent manner in BSCs. In addition, 1 mM NaB increased the mitochondrial ROS level, decreased the mitochondrial membrane potential (MMP), increased the number of autophagic vesicles in mitochondria, and increased the mitochondrial DNA (mtDNA) and ATP level. The effects of the mTOR pathway on BSCs were investigated. The results showed that 1 mM NaB inhibited the mRNA and protein expression of mTOR and genes AKT1, FOXO1, and EIF4EBP1 in the mTOR signaling pathway. In contrast, the addition of PP242, an inhibitor of the mTOR signaling pathway also inhibited mRNA and protein expression levels of mTOR, AKT1, FOXO1, and EIF4EBP1 and promoted mitophagy and apoptosis, which were consistent with the effect of NaB treatment. NaB might promote mitophagy and apoptosis in BSCs by inhibiting the mTOR signaling pathway. Our results would expand the knowledge of sodium butyrate on bovine skeletal muscle cell state and mitochondrial function.
丁酸钠（NaB）是短链脂肪酸之一，在肠道中大量由膳食纤维产生。最近的证据表明，NaB 诱导细胞增殖和凋亡。骨骼肌富含大量线粒体。然而，目前尚不清楚 NaB 如何作用于宿主肌细胞，以及它是否参与肌细胞中线粒体相关功能。本研究旨在探讨 NaB 处理对牛骨骼肌卫星细胞（BSC）增殖、凋亡和自噬的作用。结果表明，NaB 以时间和剂量依赖的方式抑制 BSCs 的增殖，促进 BSCs 的凋亡，并促进自噬。此外，1mM NaB 增加线粒体 ROS 水平，降低线粒体膜电位（MMP），增加线粒体自噬小泡数量，增加线粒体 DNA（mtDNA）和 ATP 水平。研究了 mTOR 通路对 BSCs 的影响。结果表明，1mM NaB 抑制 mTOR 及其下游基因 AKT1、FOXO1 和 EIF4EBP1 的 mRNA 和蛋白表达。相反，mTOR 信号通路抑制剂 PP242 的添加也抑制了 mTOR、AKT1、FOXO1 和 EIF4EBP1 的 mRNA 和蛋白表达水平，并促进自噬和凋亡，这与 NaB 处理的效果一致。NaB 可能通过抑制 mTOR 信号通路促进 BSCs 中的自噬和凋亡。我们的研究结果将扩展对丁酸钠在牛骨骼肌细胞状态和线粒体功能方面的认识。
