Huang M T, Lou Y R, Ma W, Newmark H L, Reuhl K R, Conney A H
Department of Chemical Biology and Pharmacognosy, College of Pharmacy, Rutgers, State University of New Jersey, Piscataway 08855-0789.
Cancer Res. 1994 Nov 15;54(22):5841-7.
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.
姜黄素(二阿魏酰甲烷)是从姜黄属植物姜黄的根茎中提取的一种黄色色素,是姜黄的主要成分,常用作香料和食品着色剂。评估了在AIN 76A饮食中添加商业级姜黄素(77%姜黄素、17%去甲氧基姜黄素和3%双去甲氧基姜黄素)对致癌物诱导的小鼠前胃、十二指肠和结肠肿瘤发生的抑制作用。经口给予饮食中的商业级姜黄素可抑制A/J小鼠中苯并(a)芘诱导的前胃肿瘤发生、C57BL/6小鼠中N-乙基-N'-硝基-N-亚硝基胍诱导的十二指肠肿瘤发生以及CF-1小鼠中偶氮甲烷(AOM)诱导的结肠肿瘤发生。给小鼠喂食饮食中的商业级姜黄素的时间为:(a)在给予致癌物前2周、期间及之后1周(启动期);(b)在致癌物处理后1周直至实验结束(启动后期);或(c)在启动期和启动后期。在启动期给予饮食中0.5 - 2.0%的商业级姜黄素可使每只小鼠苯并(a)芘诱导的前胃肿瘤数量减少51 - 53%,在启动后期给予时减少47 - 67%。在启动后期给予饮食中0.5 - 2.0%的商业级姜黄素可使每只小鼠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%。在启动期和启动后期均给予饮食中0.5 - 4.0%的商业级姜黄素可使每只小鼠AOM诱导的结肠肿瘤数量减少51 - 62%。在启动期给予饮食中2%的商业级姜黄素可使每只小鼠AOM诱导的结肠肿瘤数量减少66%,在启动后期给予时减少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。给AOM处理的小鼠喂食饮食中的纯姜黄素或商业级姜黄素会导致结肠肿瘤的发生,与AOM处理的对照组小鼠相比,肿瘤数量和大小通常较少。这些结果表明,姜黄素不仅抑制了每只小鼠的肿瘤数量和患肿瘤小鼠的百分比,还减小了肿瘤大小。对肿瘤的组织病理学检查表明,饮食中的姜黄素抑制了前胃乳头瘤和鳞状细胞癌的数量以及十二指肠和结肠腺瘤和腺癌的数量。