为了为健脾汤(JP)的抗癌恶病质效应提供全面的证据，并探讨其抗癌恶病质机制。使用结肠癌(CT26)诱导癌症恶病质(CC)的小鼠模型，研究JP联合醋酸甲羟孕酮(MPA)的抗恶病质效应。将36只小鼠均匀分为6组：正常对照组、CC组、MPA (100 mg・kg-1・d-1)组、MPA + 低剂量 (20 mg・kg-1・d-1) JP (L-JP)组、MPA + 中剂量 (30 mg・kg-1・d-1) JP (M-JP)组和 MPA + 高剂量 (40 mg・kg-1・d-1) JP (H-JP)组。成功建模后，小鼠经灌胃给药11天。从移植开始的第8天起，每两天测量和记录体重和肿瘤体积。收集和称量小鼠的肝脏、心脏、脾脏、肺、肾脏、肿瘤和腓肠肌，观察肿瘤的病理变化，计算腓肠肌的横截面积。通过Western blot测量腓肠肌中STAT3和E3泛素化酶的蛋白表达。此外，建立了体外C2C12肌管形成模型，研究JP在阻止地塞米松诱导的肌肉萎缩中的作用。体外实验分为对照组、模型组和JP血清组。在给药2天后，进行显微照片拍摄，并计算肌管直径。进行Western blot检测C2C12肌肉中STAT3和E3泛素化酶蛋白的表达。JP联合MPA恢复了肿瘤引起的体重减轻(P<0.05, vs. CC)和肌纤维大小(P<0.01, vs. CC)。从机制上讲，JP减少了肿瘤引起的肌肉萎缩中与萎缩相关的MuRF1和MAFbx蛋白的表达(P<0.05, vs. CC)。此外，在体外用地塞米松处理的C2C12肌肉中，JP减少了与萎缩相关的MuRF1和MAFbx蛋白以及p-STAT3磷酸化的表达(P<0.05或P<0.01, vs. 模型组)。JP联合MPA治疗可以恢复肿瘤引起的恶病质状况。此外，JP联合MPA对肿瘤引起的恶病质的深远影响可能是由于其抑制肌肉蛋白溶解（E3泛素化酶系统）。© 2023年。中国中西医结合杂志社和德国斯普林格出版社，斯普林格自然出版集团的一部分。

To provide comprehensive evidence for the anti-cancer cachexia effect of Jianpi Decoction (JP) and to explore its mechanism of anti-cancer cachexia.A mouse model of colon cancer (CT26)-induced cancer cachexia (CC) was used to investigate the anti-CC effect of JP combined with medroxyprogesterone acetate (MPA). Thirty-six mice were equally divided into 6 groups: normal control, CC, MPA (100 mg•kg-1•d-1), MPA + low-dose (20 mg•kg-1•d-1) JP (L-JP), MPA + medium-dose (30 mg•kg-1•d-1) JP (M-JP), and MPA + high-dose (40 mg•kg-1•d-1) JP (H-JP) groups. After successful modeling, the mice were administered by gavage for 11 d. The body weight and tumor volume were measured and recorded every 2 d starting on the 8th day after implantation. The liver, heart, spleen, lung, kidney, tumor and gastrocnemius muscle of mice were collected and weighed. The pathological changes of the tumor was observed, and the cross-sectional area of the gastrocnemius muscle was calculated. The protein expressions of STAT3 and E3 ubiquitinase in the gastrocnemius muscle were measured by Western blot. In addition, an in vitro C2C12 myotube formation model was established to investigate the role of JP in hindering dexamethasone-induced muscle atrophy. In vitro experiments were divided into control, model, and JP serum groups. After 2-d administration, microscopic photographs were taken and myotube diameters were calculated. Western blot was performed to measure the protein expressions of STAT3 and E3 ubiquitinase.JP combined with MPA restored tumor-induced weight loss (P<0.05, vs. CC) and muscle fiber size (P<0.01, vs. CC). Mechanistically, JP reduced the expression of atrophy-related proteins MuRF1 and MAFbx in tumor-induced muscle atrophy in vivo (P<0.05, vs. CC). In addition, JP reduced the expression of atrophy-related proteins MuRF1 and MAFbx and p-STAT3 phosphorylation (P<0.05 or P<0.01 vs. model group) in C2C12 myotubes treated with dexamethasone in vitro.Administration of JP combined with MPA restores tumor-induced cachexia conditions. In addition, the profound effect of JP combined with MPA on tumor-induced cachexia may be due to its inhibition of muscle proteolysis (E3 ubiquitinase system).© 2023. The Chinese Journal of Integrated Traditional and Western Medicine Press and Springer-Verlag GmbH Germany, part of Springer Nature.