Henschel L D V, Lima M E R de, Fagundes F C, Horlem T, Zazula M F, Naliwaiko K, Fernandes L C
Laboratório de Metabolismo Celular, Departamento de Fisiologia, Setor de Ciências Biológicas, Universidade Federal do Paraná, Curitiba, PR, Brasil.
Laboratório de Plasticidade Morfofuncional, Departamento de Biologia Celular e Molecular, Setor de Ciências Biológicas, Universidade Federal do Paraná, Curitiba, PR, Brasil.
Braz J Med Biol Res. 2025 Jan 31;58:e14060. doi: 10.1590/1414-431X2024e14060. eCollection 2025.
Cancer is the second leading cause of death worldwide. Cancer cachexia is a multifactorial catabolic syndrome responsible for almost one third of cancer-related deaths. Drug repurposing has been used in oncological research and drugs like clenbuterol and metformin seem to be reasonable candidates in the context of cancer cachexia, because the former is a β2-agonist that stimulates muscle gain and the latter has anti-inflammatory properties. The aim of this study was to assess the effects of a short-term treatment with metformin and clenbuterol, isolated or combined, on tumor growth and cancer cachexia parameters in Walker 256 tumor-bearing rats, a model of cancer cachexia. To this end, Wistar rats were separated into 8 groups and 4 of them were injected with Walker 256 tumor cells (W groups). Control (C) and W groups received the following treatments: metformin (M), clenbuterol (Cb), or metformin combined with clenbuterol (MCb). Body and tumor weight, metabolic parameters, and oxidative damage in the tumor were assessed. Compared to the C group, the W group showed body weight loss, hypoglycemia, hyperlactatemia, and hypertriacylglycerolemia. None of the treatments could reverse body weight loss, although they reversed the alterations of the assessed plasma metabolic parameters. Surprisingly, only clenbuterol alone reduced tumor weight. Hydrogen peroxide production and lipid peroxidation in tumor tissue was increased in this group. In conclusion, metformin and clenbuterol ameliorated metabolic cachexia parameters in Walker tumor-bearing rats, but only clenbuterol reduced the tumor weight, probably, through a lipid peroxidation-dependent cell death.
癌症是全球第二大死因。癌症恶病质是一种多因素分解代谢综合征,几乎占癌症相关死亡人数的三分之一。药物重新利用已应用于肿瘤学研究,在癌症恶病质背景下,克伦特罗和二甲双胍等药物似乎是合理的候选药物,因为前者是一种β2激动剂,可刺激肌肉增长,而后者具有抗炎特性。本研究的目的是评估短期使用二甲双胍和克伦特罗单独或联合治疗对Walker 256荷瘤大鼠肿瘤生长和癌症恶病质参数的影响,Walker 256荷瘤大鼠是一种癌症恶病质模型。为此,将Wistar大鼠分为8组,其中4组注射Walker 256肿瘤细胞(W组)。对照组(C组)和W组接受以下治疗:二甲双胍(M组)、克伦特罗(Cb组)或二甲双胍联合克伦特罗(MCb组)。评估了体重、肿瘤重量、代谢参数和肿瘤中的氧化损伤。与C组相比,W组出现体重减轻、低血糖、高乳酸血症和高三酰甘油血症。尽管所有治疗都逆转了所评估的血浆代谢参数的改变,但没有一种治疗能够逆转体重减轻。令人惊讶的是,只有单独使用克伦特罗可降低肿瘤重量。该组肿瘤组织中的过氧化氢生成和脂质过氧化增加。总之,二甲双胍和克伦特罗改善了Walker荷瘤大鼠的代谢恶病质参数,但只有克伦特罗降低了肿瘤重量,可能是通过脂质过氧化依赖性细胞死亡实现的。