短期肿瘤发展方案,作为化学预防药物研究的一个选择

M. S. Cid-Gallegos, X. Sánchez-Chino, I. Álvarez-González, E. Madrigal Bujaidar, V. R. Vásquez-Garzón, Rafael Baltiérrez Hoyos, C. Jiménez Martínez
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引用次数: 0

摘要

导读:结肠癌的诊断通常较晚;因此,有必要寻找预防方案。体内模型是评估化学预防药物的一种选择,主要基于诱导和促进致癌作用;然而,他们需要很长时间。本工作旨在评价并提出一种短时间内具有肿瘤表现的致癌模型,以证明化学预防化合物的有效性。方法:用偶氮氧甲烷(AOM)和葡聚糖硫酸钠(DSS)诱导3组(n = 7)雄性BALB/c小鼠结肠癌。诱导后14周评估损伤。方案为:1)P1: 2次AOM注射和2个DSS周期,剂量为1.5%,持续5天,周期之间休息3天;2) P2:注射1次AOM和2个DSS周期,2%剂量,7天,休息5天;3)P3:注射1次AOM和2个DSS周期,2%剂量,4天,休息4天。阴性对照为平行对照,P0:随机注射生理盐水1次。测定体重、疾病活动指数(DAI)、生存率、肿瘤发生率、血脂和蛋白质氧化。结果:P2在评估体征中表现出更严重的症状(肿瘤发生率100%,结肠重长比101.68±2.99 mg/cm),生存率低(43%)。P1的死亡率较低(14%),肿瘤发病率较低(83%),与P2无显著差异。P3病变程度较轻(33%肿瘤发生率)。此外,三种方案均出现脂质氧化(0.4 ~ 0.58 ng/μg蛋白质)和蛋白质氧化(0.6 ~ 1 ng/μg蛋白质)。P1和P3诱导方案的死亡率较低,体重减轻,DAI可接受,体重/长度比高于阴性对照组和肿瘤的存在。讨论:使用AOM (10mg/kg)联合DSS(1.5-2 %)是评估感兴趣化合物、炎症体征、脂质和蛋白质氧化的致癌作用的合适模型,并且存活数足以进行统计分析,从而得出准确的结论。因此,P1和P3是可用于化学预防分析的方案,结果令人满意。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protocol for short-term tumor development, as an option for the study of chemopreventive agents
Introduction: Colon cancer diagnosis is usually performed late; so, it is necessary to search for prevention options. In vivo models are an option for the evaluation of chemopreventive agents, which are based mainly on the induction and promotion of carcinogenesis; however, they take a long time. This work aimed to evaluate and propose a carcinogenesis model, with tumor manifestation in a short time to prove the efficacy of chemopreventive compounds. Method: Colon carcinogenesis was induced in three groups (n = 7) male BALB/c mice with azoxymethane (AOM) and dextran sodium sulfate (DSS). The damage was assessed 14 weeks after the induction. Protocols were: 1) P1: two AOM injections and two DSS cycles at 1.5 % for five days, with three resting days between cycles; 2) P2: one AOM injection and two DSS cycles at 2 % for seven days with five rest days, and 3) P3: one AOM injection and two DSS cycles at 2 % for four days, with four resting days. Negative control was used in parallel, P0: with one injection of saline solution and water ad libitum. Weight, disease activity index (DAI), survival, tumor incidence, lipids, and protein oxidation were determined. Results: P2 showed greater severity in the assessed signs (100 % tumor incidence, colon weight/length ratio 101.68 ± 2.99 mg/cm), with low survival (43 %). P1 depicted lower mortality (14 %) and 83 % tumor incidence, without a significant difference to P2. P3 developed the disease but to a lesser degree (33 % tumor incidence). Furthermore, the three protocols showed lipid oxidation (0.4-0.58 ng/μg of protein) and proteins oxidation (0.6-1 ng/μg of protein). The P1 and P3 induction protocols presented less mortality, weight loss, and acceptable DAI, a weight/length ratio higher than the negative control and presence of tumors. Discussion: The use of AOM (10mg/kg) combined with DSS (1.5-2 %) are suitable models to evaluate the carcinogenic effect of compounds of interest, inflammation signs, lipids and proteins oxidation and a survival number adequate to perform the statistical analysis leading to accurate conclusions. Therefore, P1 and P3 are protocols that can be used in chemoprevention assays with satisfactory results.
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