Cancer cachexia is a metabolic disease involving multiple organs, which is accompanied by the depletion of muscle tissue and is associated with ~20% of cancer‑related deaths. Muscle wasting is a critical factor in cancer cachexia. β‑carotene (BC) has been shown to increase muscle mass and hypertrophy in healthy mice. However, its effects on muscle tissue dysregulation in cancer cachexia have yet to be studied. In the present study, 5‑week‑old male C57BL/6J mice were injected with 1x10⁶ Lewis lung carcinoma (LLC) cells to induce cancer cachexia; then the mice were administered BC (4 or 8 mg/kg) for 22 days to assess its effects on muscle atrophy in the gastrocnemius muscles. The effects of BC on inflammatory cytokines, myogenesis and muscle atrophy were evaluated using C2C12 myotubes treated with LLC‑conditioned media. BC supplementation significantly suppressed tumor growth, inflammatory cytokines, and hepatic gluconeogenesis in the LLC‑induced cancer cachexia mouse model, while also improving muscle weight and grip strength. These effects are considered to be mediated by the PI3K/Akt pathway and through regulation of muscle atrophy. Moreover, BC treatment was associated with the recovery of LLC‑conditioned media‑induced muscle differentiation deficits and muscle atrophy in C2C12 myotubes. These findings indicate BC as a potential novel therapeutic agent for cancer cachexia.

中文翻译：

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β-胡萝卜素通过调节肌生成和肌肉萎缩来减轻癌症恶病质中的肌肉萎缩。

癌症恶病质是一种涉及多个器官的代谢性疾病，伴有肌肉组织耗竭，约 20% 的癌症相关死亡与癌症相关。肌肉萎缩是癌症恶病质的一个关键因素。β-胡萝卜素（BC）已被证明可以增加健康小鼠的肌肉质量和肥大。然而，其对癌症恶病质肌肉组织失调的影响仍有待研究。在本研究中，5周大的雄性C57BL/6J小鼠被注射1x10 ⁶ Lewis肺癌(LLC)细胞以诱导癌症恶病质；然后给小鼠注射 BC（4 或 8 mg/kg）22 天，以评估其对腓肠肌肌肉萎缩的影响。使用经过 LLC 条件培养基处理的 C2C12 肌管评估 BC 对炎症细胞因子、肌生成和肌肉萎缩的影响。在 LLC 诱导的癌症恶病质小鼠模型中，BC 补充剂显着抑制了肿瘤生长、炎症细胞因子和肝脏糖异生，同时还改善了肌肉重量和握力。这些效应被认为是由 PI3K/Akt 通路和肌肉萎缩的调节介导的。此外，BC 治疗与 LLC 条件培养基诱导的 C2C12 肌管肌肉分化缺陷和肌肉萎缩的恢复相关。这些发现表明BC是一种潜在的新型癌症恶病质治疗剂。