论文部分内容阅读
目的 建立一种癌性恶病质动物模型 ,并观察其营养指标和体液因子的变化。方法 将 2 4只雄性BALB/c小鼠随机分为对照和荷瘤两组 ,荷瘤组动物皮下种植小鼠结肠腺癌 2 6细胞悬液 (1× 10 6个 /只 )。接种后监测两组小鼠的体重 ,摄食量和皮下肿瘤大小。 16d后测量血清中葡萄糖、总蛋白、白蛋白、甘油三酯和胆固醇浓度以及皮质醇、肿瘤坏死因子 α(TNF α)、白细胞介素 6(IL 6)水平。结果 两组小鼠食物摄入差异无显著性 (P >0 .0 5 ) ,16d后对照组和荷瘤组去瘤体重分别为 (2 4.88± 1.78)、(19.73± 1.3 7)g ,两者之间差异有非常显著性 (P <0 .0 1)。两组小鼠血清葡萄糖浓度分别为 (8.10± 1.18)、(4 .2 8± 0 .68)mmol/L ,胆固醇浓度分别为 (2 .86± 0 .2 5 )、(4 .5 6± 1.5 8)mmol/L ,皮质醇浓度分别为 (0 .0 4± 0 .0 2 )、(0 .17± 0 .0 4) μmol/L。对照组未测出TNF α和IL 6活性 ,而荷瘤组TNF α和IL 6浓度分别为 (10 5 .0 7± 2 7.5 6)ng/L和 (2 .62± 1.3 8) μg/L ,两组间血糖、胆固醇、皮质醇、TNF α以及IL 6的差异均有非常显著性 (P <0 .0 1)。结论 该模型成功复制了癌性恶病质 ,动物存在显著的营养不良和代谢紊乱 ,是研究癌性恶病质发生机制及其调控措施的较理想平台。
Objective To establish an animal model of cancerous cachexia and observe the changes of its nutritional indexes and humoral factors. Methods Twenty-four male BALB / c mice were randomly divided into control group and tumor-bearing group. The tumor-bearing group received 2 × 10 6 colon adenocarcinoma colonies per mouse. The weight, food intake and subcutaneous tumor size of the two groups of mice were monitored after inoculation. Serum levels of glucose, total protein, albumin, triglyceride and cholesterol as well as cortisol, tumor necrosis factor α (TNF α) and interleukin 6 (IL 6) were measured after 16 days. Results There was no significant difference in food intake between the two groups (P> 0.05). After 16 days, the tumor weight of the control group and the tumor-bearing group were (2.88 ± 1.78) and (19.73 ± 1.37) g There was a significant difference between the two groups (P <0.01). Serum glucose concentrations in the two groups were (8.10 ± 1.18) and (4.2 ± 0.868) mmol / L, respectively, and cholesterol concentrations were (2.86 ± 0.55 and 4.56 ± 1.58) mmol / L and cortisol concentrations (0. 04 ± 0. 02) and (0 .17 ± 0. 0 4) μmol / L, respectively. The TNFα and IL-6 activities were not detected in the control group, while the tumor-bearing group TNFα and IL-6 concentrations were (105.07 ± 2 7.56) ng / L and (2.62 ± 1.3 8) μg / L There were significant differences in blood glucose, cholesterol, cortisol, TNFα and IL-6 between the two groups (P <0.01). Conclusion The model successfully replicates cancerous cachexia, and there are significant malnutrition and metabolic disorders in animals. It is an ideal platform to study the mechanism of carcinogenesis and regulation of cancerous cachexia.