Inhibitory effects of dietary curcumin on forestomach, duodenal, and colon carcinogenesis in mice.
Inhibitory effects of dietary curcumin on forestomach, duodenal, and colon carcinogenesis in mice.
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发表时间：
1994-11
期刊：
影响因子：
11.2
通讯作者：
Mou-tuan Huang;Y. Lou;Wei Ma;H. Newmark;K. Reuhl;A. Conney
中科院分区：
文献类型：
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作者：
Mou-tuan Huang;Y. Lou;Wei Ma;H. Newmark;K. Reuhl;A. Conney
姜黄素（二阿魏酰甲烷），一种从姜黄（Curcuma longa Linn.）是姜黄的主要成分，通常用作香料和食品着色剂。评价了在AIN 76 A饮食中饲喂商业级姜黄素（77%姜黄素、17%脱甲氧基姜黄素和3%双脱甲氧基姜黄素）对小鼠前胃、十二指肠和结肠中致癌物诱导的肿瘤发生的抑制作用。给药p.o.在A/J小鼠中，商业级姜黄素抑制苯并（a）芘诱导的前胃肿瘤发生，在C57 BL/6小鼠中抑制N-乙基-N '-硝基-N-亚硝基胍诱导的十二指肠肿瘤发生，在CF-1小鼠中抑制氧化偶氮甲烷（AOM）诱导的结肠肿瘤发生。在以下时间点给予小鼠膳食商业级姜黄素：（a）致癌物给药前2周、给药期间和给药后1周（在启动期间）;（B）致癌物给药后1周直至实验结束（在启动后期间）;或（c）在启动和启动后期间。在饮食中喂食0.5-2.0%的商业级姜黄素可使每只小鼠的苯并（a）芘诱导的前胃肿瘤数量减少51-53%，当在起始期给药时，减少47-67%。当在起始后阶段给药时，在饮食中喂食0.5-2.0%商业级姜黄素可使每只小鼠的N-乙基-N '-硝基-N-亚硝基胍诱导的十二指肠肿瘤数量减少47-77%。在开始和开始后阶段，在饮食中给予0.5-4.0%的商业级姜黄素使每只小鼠的AOM诱导的结肠肿瘤数量减少了51- 62%。在饮食中加入2%的商业级姜黄素，在开始阶段喂食时，每只小鼠AOM诱导的结肠肿瘤数量抑制了66%，在开始后阶段喂食时，抑制了25%。商业级姜黄素抑制AOM诱导的结肠肿瘤发生的能力与纯姜黄素（纯度大于98%）相当。向AOM处理的小鼠施用饮食中的纯或商业级姜黄素导致结肠肿瘤的发展，与对照组的AOM处理的小鼠相比，结肠肿瘤的数量和大小通常较小。这些结果表明，姜黄素不仅抑制了每只小鼠的肿瘤数量和肿瘤小鼠的百分比，而且还减小了肿瘤大小。肿瘤的组织学检查表明，饮食姜黄素抑制乳头状瘤和鳞状细胞癌的前胃以及腺瘤和腺癌的十二指肠和结肠的数量。
Curcumin (diferuloylmethane), a yellow pigment that is obtained from the rhizomes of Curcuma longa Linn., is a major component of turmeric and is commonly used as a spice and food-coloring agent. The inhibitory effects of feeding commercial grade curcumin (77% curcumin, 17% demethoxycurcumin, and 3% bisdemethoxycurcumin) in AIN 76A diet on carcinogen-induced tumorigenesis in the forestomach, duodenum, and colon of mice were evaluated. Administration p.o. of commercial grade curcumin in the diet inhibited benzo(a)pyrene-induced forestomach tumorigenesis in A/J mice, N-ethyl-N'-nitro-N-nitrosoguanidine-induced duodenal tumorigenesis in C57BL/6 mice, and azoxymethane (AOM)-induced colon tumorigenesis in CF-1 mice. Dietary commercial grade curcumin was given to mice at: (a) 2 weeks before, during, and for 1 week after carcinogen administration (during the initiation period); (b) 1 week after carcinogen treatment until the end of the experiment (during the postinitiation period); or (c) during both the initiation and postinitiation periods. Feeding 0.5-2.0% commercial grade curcumin in the diet decreased the number of benzo(a)pyrene-induced forestomach tumors per mouse by 51-53% when administered during the initiation period and 47-67% when administered during the postinitiation period. Feeding 0.5-2.0% commercial grade curcumin in the diet decreased the number of N-ethyl-N'-nitro-N-nitrosoguanidine-induced duodenal tumors per mouse by 47-77% when administered during the postinitiation period. Administration of 0.5-4.0% commercial grade curcumin in the diet both during the initiation and postinitation periods decreased the number of AOM-induced colon tumors per mouse by 51-62%. Administration of 2% commercial grade curcumin in the diet inhibited the number of AOM-induced colon tumors per mouse by 66% when fed during the initiation period and 25% when fed during the postinitiation period. The ability of commercial grade curcumin to inhibit AOM-induced colon tumorigenesis is comparable to that of pure curcumin (purity greater than 98%). Administration of pure or commercial grade curcumin in the diet to AOM-treated mice resulted in development of colon tumors which were generally smaller in number and size as compared to the control group of AOM-treated mice. These results indicate that not only did curcumin inhibit the number of tumors per mouse and the percentage of mice with tumors but it also reduced tumor size. Histopathological examination of the tumors showed that dietary curcumin inhibited the number of papillomas and squamous cell carcinomas of the forestomach as well as the number of adenomas and adenocarcinomas of the duodenum and colon.