机构地区:[1]上海交通大学附属第六人民医院普外科,200233 [2]上海市第十人民医院普外科,200072
出 处:《中华临床营养杂志》2014年第3期171-177,共7页Chinese Journal of Clinical Nutrition
基 金:国家自然科学基金(81230057);国家高技术研究发展计划(863计划)(SS2014AA020803);上海市市级医院新兴前沿技术联合攻关项目(SHDC12012106)
摘 要:目的用1,2-二甲基肼诱导大鼠肠道肿瘤,同时观察高脂对1,2-二甲基肼诱导大肠肿瘤的影响。方法Westar大鼠50只,鼠龄7周,根据不同饮食及是否腹腔注射二甲基肼将大鼠分为4组:标准饮食对照组(n=10)、标准饮食±二甲肼诱导成瘤(SDT,n=15)组、高脂饮食对照组(n=10)、高脂饮食±二甲肼诱导成瘤(HFDT,n=15)组。实验18周后处死大鼠,酶联免疫吸附法检测大鼠血清甘油三酯(TG)、肿瘤坏死因子(TNF)-α及结肠TNF-α、白介素-6(IL-6)水平;取出肠道,观察肿瘤部位、数量、大小等,制作病理切片,观察组织学改变,免疫组织化学法检测TNF-α、Ki-67在正常组织、肿瘤中的分布。结果实验结束时SDT组大鼠死亡率20.00%、成瘤率75.00%、荷瘤率117%,HFDT组大鼠死亡率26.67%、成瘤率81.82%、荷瘤率191%,SDT组和HFDT组死亡率、成瘤率(P=0.545)及荷瘤率(χ^2=1.343,P=0.247)差异均无统计学意义。SDT组中肿瘤平均体积〉0.05cm^3个数占28.57%,HFDT组中肿瘤平均体积〉0.05cm^2个数占66.67%,两组肿瘤平均体积差异具有统计学意义(P=0.030)。高脂饮食大鼠血清TG[(1.39±0.31)mmol/L]、TNF-α[(124.80±21.69)ng/L]较标准饮食大鼠血清TG[(0.46±0.20)mmol/L]、TNF-α[(85.83±17.45)ng/L]显著升高(P值均=0.000)。高脂饮食大鼠结肠黏膜TNF-α[(6.22±0.63)ng/g]、IL-6[(13.50±0.67)ng/g]较标准饮食大鼠结肠黏膜TNF-α[(2.33±0.44)ng/g]、IL-6[(7.31±0.41)ng/g]显著升高(P=0.020,P=0.000);高脂饮食对照组Ki-67阳性表达率40%,较标准饮食对照组10%显著升高(P=0.028);HFDT组Ki-67阳性表达率90.48%较SDT组50%显著升高(P=0.015)。结论高脂饮食可能通过导致大鼠血清TG、TNF-α上升,上调结肠黏膜炎症因子TNF-α、IL-6及增殖细胞�Objective To explore the effect of fat on 1,2-dimethylhydrazine (DMH) -induced colon tumors. Methods A total of 50 7-week-old male Wistar rats were further divided into four groups: standard diet feed control group ( n = 10), standard diet feed plus DMH-induced tumor group ( SDT, n = 15 ), high-fat diet feed control group ( n = 10) and high-fat diet feed plus DMH-induced tumor group ( HFDT, n = 15 ). Rats were killed 18 weeks later, and enzyme-linked immunosorbent assay was used to detect serum triglyceride, tumor necrosis factor (TNF-ot), and colonic TNF-α, interleukin-6. After the intestinal tracts were removed, the location, amount, and size of the tumors were observed. The pathological changes of the tissue sections were observed, and the distributions of TNF-α and Ki-67 in the normal tissues and tumors were detected by immunohistochemistry. Results Upon the completion of the study, the mortality rate of rats was 20.00% in the SDT group and 26. 67% in the HFDT group, the tumor formation rate was 75.00% in the SDT group and 81.82% in the HFDT group, and the tumor-bearing rate was 117% in the SDT group and 191% in the HFDT group. No statistical significance difference between the two groups in mortality rate, tumor formation rate ( P = 0. 545 ) and tumor bearing rate (χ^2 = 1. 343, P = 0. 247 ). The average tumor volume was significantly different between the standard diet feed control group and high-fat diet feed control group (28.57% vs 66. 67% , P = 0. 030). Also, the serum triglyceride and TNF-α levels significantly differed between the SDT group and HFDT group [TG ( 1.39 ±0. 31 ) mmol/L and TNF-α ( 124. 80 ±21.69) ng/L in the HFDT group and TG (0. 46 ±0. 20) mmol/L and TNF-α (85.83 ± 17.45) ng/L in the SDT group] (P =0. 000). The expressions of TNF-α, IL-6, and Ki-67 in colonic mucosa were significantly higher in the high-fat diet feed control group than in the standard diet feed control group [ TNF-α: (6. 22 ±0. 63) ng/g vs (2.
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