To develop a more effective and safer treatment for sarcopenia, this research investigated the anti-sarcopenia mechanism of Milk Fat Globule Epidermal Growth Factor Ⅷ (MFG-E8) from the liver function and metabolism in sarcopenic model rat. After 4 weeks nutritional intervention experiment, MFG-E8 can significantly increase the gastrocnemius mass in rat. The mechanism of MFG-E8 in improving sarcopenia was related to its promotional capacity to the activities of superoxide dismutase (SOD) activity in serum, Glutamic-oxaloacetic transaminase (GOT) and glutamic-pyruvic transaminase (GPT) in liver. Meanwhile, MFG-E8 could also down-regulate obesity-related indicators, such as triglyceride (TG) and Non-esterified fatty acid (NEFA). The analysis of liver and gastrocnemius histopathology found that MFG-E8 could reduce the accumulation of fatty vesicles, improve liver function, thereby alleviating gastrocnemius tissue inflammation. In vitro experiments, myoblasts obtained from gastrocnemius tissue showed that MFG-E8 could reduce mitochondrial autophagy and inhibit cell apoptosis. In addition, MFG-E8 could up-regulate the phosphorylation level of PI3K via activating PI3K/Akt signaling pathway in gastrocnemius tissue, and promote the formation of muscle fibers, thereby increasing muscle mass. Moreover, MFG-E8 could also promote the formation of neuromuscular junctions by up-regulating the mRNA and protein expression of MusK in gastrocnemius.

为了开发一种更有效，更安全的少肌症治疗方法，本研究从少肌症模型大鼠的肝功能和代谢研究了乳脂球表皮生长因子Ⅷ（MFG-E8）的抗少肌症机制。经过4周的营养干预实验，MFG-E8可以显着增加大鼠腓肠肌的质量。MFG-E8改善少肌症的机制与其对血清中超氧化物歧化酶（SOD）活性，谷氨酸-草酰乙酸转氨酶（GOT）和谷氨酸-丙酮酸转氨酶（GPT）的促进能力有关。同时，MFG-E8还可以下调与肥胖相关的指标，例如甘油三酸酯（TG）和非酯化脂肪酸（NEFA）。肝和腓肠肌组织病理学分析发现，MFG-E8可以减少脂肪囊泡的积累，在体外实验中，从腓肠肌组织获得的成肌细胞显示MFG-E8可以减少线粒体自噬并抑制细胞凋亡。此外，MFG-E8可以通过激活腓肠肌组织中的PI3K / Akt信号通路来上调PI3K的磷酸化水平，并促进肌肉纤维的形成，从而增加肌肉质量。此外，MFG-E8还可以通过上调腓肠肌MusK的mRNA和蛋白表达来促进神经肌肉接头的形成。