Park Jeongjin, Koo Gi-Bang, Kwon Han Ol, Kim Jong Han, Jun Woojin
Division of Food and Nutrition and Human Ecology Research Institute, Chonnam National University, Gwangju, Republic of Korea.
Korea Ginseng Corporation Research Institute, Korea Ginseng Corporation, Gwacheon, Republic of Korea.
J Med Food. 2025 Jan;28(1):58-67. doi: 10.1089/jmf.2024.k.0220. Epub 2024 Dec 30.
Here, we investigated whether a mixture of and (1:3, KGC01CE) could suppress muscle atrophy in HO-induced C2C12 cells and dexamethasone-injected mice. Our results revealed that KGC01CE effectively safeguarded against HO-induced muscle atrophy in C2C12 cells compared with the same mixture at other ratios. We demonstrated that dexamethasone elicited oxidative stress in muscle tissue and decreased the grip strength and cross-sectional areas of muscle fibers; however, oral administration of KGC01CE (1:3) suppressed these dexamethasone-induced changes. Furthermore, oral KGC01CE (1:3) administration suppressed the expression of protein degradation-associated factors, myostatin, muscle RING finger 1, and atrogin-1 in muscle tissue from dexamethasone-injected mice. Oral KGC01CE administration stimulated protein synthesis by stimulating the PI3K/Akt/mTOR pathway in muscle tissue from dexamethasone-injected mice. These findings indicate that KGC01CE can suppress dexamethasone injection-induced muscle atrophy by inhibiting protein degradation and promoting muscle hypertrophy. Therefore, KGC01CE supplementation helps prevent muscle atrophy in mice and may be beneficial against various components of muscle atrophy.
在此,我们研究了[具体成分1]和[具体成分2]的混合物(1:3,KGC01CE)是否能抑制缺氧诱导的C2C12细胞和地塞米松注射小鼠的肌肉萎缩。我们的结果显示,与其他比例的相同混合物相比,KGC01CE能有效防止缺氧诱导的C2C12细胞肌肉萎缩。我们证明地塞米松在肌肉组织中引发氧化应激,并降低握力和肌肉纤维横截面积;然而,口服KGC01CE(1:3)可抑制这些地塞米松诱导的变化。此外,口服KGC01CE(1:3)可抑制地塞米松注射小鼠肌肉组织中与蛋白质降解相关因子、肌肉生长抑制素、肌肉环指蛋白1和肌肉萎缩相关基因1的表达。口服KGC01CE通过刺激地塞米松注射小鼠肌肉组织中的PI3K/Akt/mTOR途径来促进蛋白质合成。这些发现表明,KGC01CE可通过抑制蛋白质降解和促进肌肉肥大来抑制地塞米松注射诱导的肌肉萎缩。因此,补充KGC01CE有助于预防小鼠肌肉萎缩,可能对肌肉萎缩的各个方面有益。