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(刺果苏木)朱西厄果实提取物可减轻癌症恶病质中的肌肉萎缩。

Extract of (Thunba.) Jussieu Fruit Reduces Muscle Atrophy in Cancer Cachexia.

作者信息

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

机构信息

Department of Anatomy Korea University College of Medicine Seoul Korea.

Biodiversity Research Institute, Clean Bio Business Division, Jeju Technopark Jeju Korea.

出版信息

Food Sci Nutr. 2025 Jul 16;13(7):e70624. doi: 10.1002/fsn3.70624. eCollection 2025 Jul.

Abstract

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.

摘要

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。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cc40/12264419/72a8f1c86693/FSN3-13-e70624-g007.jpg

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