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Sprague-Dawley大鼠皮下接种Walker 256癌肉瘤后随机分为对照组、IL-2治疗组和TNF+IL-2序贯治疗组。分别切取组织分析肿瘤及宿主肝、肌肉和整体蛋白质代谢。IL-2和TNF+IL-2组的肿瘤分段生长率(分别为17.7±2.9和23.4±3.0％/d,与对照组33.8±3.4％/d比较,P<0.05)和蛋白质合成率(分别为0.14±0.04和0.18±0.06g/d,与对照组0.56±0.14g/d比较,P<0.01)均显著降低,两组的肝蛋白质分段合成率(分别为107.7±7.1和105.0±9.1％/d,对照组79.6±6.9％/d,P<0.05)和肌肉蛋白质分段合成率(分别为15.8±1.2和13.7±1.1％/d,对照组10.7±0.7％/d,P<0.05)均增加,两组间无显著差异。三组的肿瘤蛋白质分解和整体蛋白质合成均无显著改变。本文结果表明,IL-2可致肿瘤蛋白质合成减少及宿主肝和肌肉蛋白质合成增加,但TNF与IL-2的序贯治疗并未显著增加IL-2对肿瘤和宿主蛋白质代谢的作用。
After subcutaneously inoculating Walker 256 carcinosarcoma into Sprague-Dawley rats, they were randomly divided into control group, IL-2 treatment group, and TNF+IL-2 sequential treatment group. Tissues were harvested for analysis of tumor and host liver, muscle, and overall protein metabolism. The tumor growth rates of the IL-2 and TNF+IL-2 groups were 17.7±2.9 and 23.4±3.0%/d, respectively, compared with the control group of 33.8±3.4%/d, P<0.05) and protein synthesis rates ( They were 0.14±0.04 and 0.18±0.06g/d, respectively, compared with 0.56±0.14g/d in the control group (P<0.01). Both groups had significantly lower hepatic protein fragmentation rates (107.7±7.1 and 105.0±, respectively). 9.1%/d, control group 79.6±6.9%/d, P<0.05) and muscle protein fragmentation rate (15.8±1.2 and 13.7±1.1%/d, respectively, control group 10.7±0.7%/d, P< 0.05) both increased, there was no significant difference between the two groups. There was no significant change in protein degradation and overall protein synthesis in the three groups. The results of this study indicate that IL-2 can reduce the synthesis of tumor proteins and increase the protein synthesis of liver and muscle in the host. However, the sequential treatment of TNF and IL-2 does not significantly increase the effect of IL-2 on tumor and host protein metabolism.