Noguchi Y, Makino T, Yoshikawa T, Nomura K, Fukuzawa K, Matsumoto A, Yamada T
First Department of Surgery, Yokohama City University School of Medicine, Japan.
Surg Today. 1996;26(1):36-41. doi: 10.1007/BF00311989.
This study was conducted to investigate the role of tumor necrosis factor-alpha (TNF-alpha) and interleukin-2 (IL-2) in inducing cancer cachexia, and the results were compared with those obtained from our previous study on Fisher 344 rats with methylcholanthrene-induced sarcoma. Three groups of male Fisher 344 rats received one of the following regimens: 4 x 10(4) IU of human recombinant TNF-alpha per rat per day subcutaneously (sc) for 5 consecutive days (n = 5), 3.5 x 10(5) U human recombinant IL-2 per rat per day sc for 14 consecutive days (n = 5), or normal saline (n = 5). The activities of both phosphoenolpyruvate carboxykinase (PEPCK) and malic enzyme (ME) were increased slightly in the IL-2 group. Furthermore, LPL activity was significantly increased in the adipose tissue of the TNF group and in the cardiac muscle of the IL-2 group, but not in that of the TNF group. These results show that there is a significant difference between the metabolic alterations seen in the tumor-bearing state and those induced by either TNF-alpha or IL-2 alone. Thus, it is unlikely that IL-2 or TNF-alpha is the sole mediator of cancer cachexia in this tumor and rat model.
本研究旨在探讨肿瘤坏死因子-α（TNF-α）和白细胞介素-2（IL-2）在诱发癌症恶病质中的作用，并将结果与我们之前对甲基胆蒽诱导肉瘤的Fisher 344大鼠研究所得结果进行比较。三组雄性Fisher 344大鼠接受以下方案之一：每只大鼠每天皮下注射4×10⁴国际单位人重组TNF-α，连续5天（n = 5）；每只大鼠每天皮下注射3.5×10⁵单位人重组IL-2，连续14天（n = 5）；或生理盐水（n = 5）。在IL-2组中，磷酸烯醇丙酮酸羧激酶（PEPCK）和苹果酸酶（ME）的活性均略有增加。此外，TNF组脂肪组织和IL-2组心肌中的脂蛋白脂肪酶（LPL）活性显著增加，但TNF组心肌中的LPL活性未增加。这些结果表明，荷瘤状态下所见的代谢改变与单独由TNF-α或IL-2诱导的代谢改变之间存在显著差异。因此，在该肿瘤和大鼠模型中，IL-2或TNF-α不太可能是癌症恶病质的唯一介质。
