Woo Sang Woo, Lim Pooreum, Han Jihye, Kang Ho Jin, Shim Jae Ho, Lim Jin Ju, Yoon Seon-A, Hyeon Hyejin, Ham Young-Min, Park Ji-Gweon, Jung Yong-Hwan, Kim Hyeon Soo
Department of Anatomy Korea University College of Medicine Seoul Korea.
Biodiversity Research Institute, Clean Bio Business Division, Jeju Technopark Jeju Korea.
Food Sci Nutr. 2025 Jul 16;13(7):e70624. doi: 10.1002/fsn3.70624. eCollection 2025 Jul.
Cancer cachexia is a complex syndrome involved in muscle wasting, fat depletion, fatigue, reduced appetite, and unintentional weight loss. Recent studies have suggested that natural products can prevent cancer cachexia; however, there have been no studies on the effects of fruit extract on cancer cachexia. This study aimed to identify compounds of fruit extracted from water (LJFE-W) and those extracted from 30% ethanol (LJFE-E) for cancer cachexia treatment. In vitro and in vivo models were used for C26 conditioned medium (CM)-induced C2C12 myotubes and C26 tumor-bearing mice. We demonstrated that LJFE-W and LJFE-E regulated myostatin (MSTN), E3 ligase muscle-specific RING finger protein-1 (MuRF1), and muscular atrophy fbox-1 protein (MAFbx32) expression in a CM-induced in vitro model. LJFE-E ameliorated conditioned medium-induced myotube atrophy in cultured C2C12 myotubes. In contrast, LJFE-W and LJFE-E stimulated the Akt-mTOR signaling pathway for protein synthesis in C2C12 myotubes. In animal models, the LJFE-E-injected C26 tumor-bearing group showed lower transcript-level expression of MSTN, MuRF1, and MAFbx32 in the gastrocnemius muscles than the C26 tumor-bearing group. LJFE ameliorated muscle atrophy in the cancer cachexia model by inhibiting MSTN. Thus, LJFE can be used as a supplement to cancer cachexia therapy.
癌症恶病质是一种复杂的综合征,涉及肌肉萎缩、脂肪消耗、疲劳、食欲减退和非自愿体重减轻。最近的研究表明,天然产物可以预防癌症恶病质;然而,尚未有关于水果提取物对癌症恶病质影响的研究。本研究旨在鉴定从水中提取的水果(LJFE-W)和从30%乙醇中提取的水果(LJFE-E)中用于治疗癌症恶病质的化合物。体外和体内模型用于C26条件培养基(CM)诱导的C2C12肌管和C26荷瘤小鼠。我们证明,在CM诱导的体外模型中,LJFE-W和LJFE-E调节肌生成抑制素(MSTN)、E3连接酶肌肉特异性环指蛋白-1(MuRF1)和肌肉萎缩fbox-1蛋白(MAFbx32)的表达。LJFE-E改善了培养的C2C12肌管中条件培养基诱导的肌管萎缩。相比之下,LJFE-W和LJFE-E刺激了C2C12肌管中蛋白质合成的Akt-mTOR信号通路。在动物模型中,注射LJFE-E的C26荷瘤组腓肠肌中MSTN、MuRF1和MAFbx32的转录水平表达低于C26荷瘤组。LJFE通过抑制MSTN改善了癌症恶病质模型中的肌肉萎缩。因此,LJFE可作为癌症恶病质治疗的补充剂。