Undaria pinnatifida Extracts and Alginic Acid Attenuated Muscle Atrophy in TNF-α Induced Myoblast Cells through MAFbx Signaling Cascade

S. Choi, Mina Kim, H. H. L. Lee, J. Hur
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Abstract

Muscle atrophy refers to a decrease in muscle cells due to damage to muscle fibers. It is reported that muscle atrophy is caused by heart disease, diabetes, and other chronic diseases related to aging. The purpose of this study is to reveal the inhibitory effects of seaweed extracts, which are widely consumed in Korea, and alginic acid on muscle cell damage in muscle atrophy and regeneration models. We found that seaweed extracts (U) and alginic acid (A) attenuated TNF-α-induced muscle atrophy in differentiated C2C12 myoblast cells and inhibited muscle atrophy markers such as MuRF1 and MAFbx. In addition, U and A also regulated ubiquitination marker FoxO1 protein. To confirm the muscle regeneration effect in animal tissue, cardiotoxin (CTX) was used for the regeneration model. Six hours after CTX injection, gastrocnemius muscle volume was increased compared to control. Otherwise, the muscle volume of the U and A treatment groups was not changed. U and A also upregulated regeneration markers MyHC and PGC-1α in a CTX mouse model. These results indicate that seaweed extracts and alginic acid, a seaweed component, are applicable to senile sarcopenia by inhibiting muscle loss and promoting muscle regeneration.
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裙带菜提取物和褐藻酸通过MAFbx信号级联减轻TNF-α诱导的成肌细胞的肌肉萎缩
肌肉萎缩是指由于肌肉纤维受损而导致肌肉细胞减少。据报道,肌肉萎缩是由心脏病、糖尿病和其他与衰老有关的慢性疾病引起的。本研究的目的是揭示国内广泛使用的海藻提取物和海藻酸对肌肉萎缩和再生模型中肌肉细胞损伤的抑制作用。我们发现海藻提取物(U)和褐藻酸(A)能减轻TNF-α-诱导的分化的C2C12成肌细胞的肌肉萎缩,并抑制肌肉萎缩标志物如MuRF1和MAFbx。此外,U和A还调节泛素化标记fox01蛋白。为了证实心脏毒素在动物组织中的肌肉再生作用,心脏毒素(CTX)被用于再生模型。注射CTX 6小时后,腓肠肌体积较对照组增加。除此之外,U和A治疗组肌肉体积没有变化。在CTX小鼠模型中,U和A也上调再生标志物MyHC和PGC-1α。上述结果表明,海藻提取物和海藻酸可通过抑制肌肉损失和促进肌肉再生来治疗老年性肌肉减少症。
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