Depressant Effect of Epigallocatechin-3-gallate (EGCG) on Colorectal Cancer with Dimethyl Hydrazine Induce in Colon Cancer Rats Model
|School||Nanjing University of Traditional Chinese Medicine|
|Keywords||DMH colon cancer in rats EGCG|
[Background] There has been the effect of health maintenance in record from ancient. Tea polyphenols, which account for 20%-30% of the tea’s dry weight, are polyhydroxy phenolic compounds extracted from green tea. The main components of tea polyphenols are catechins, which include several monomers such as EGCG, EGC, ECG and EC and so on.Among all the catechins,EGCG is most abundant and biological activity.Anti-tumor effects of tea polyphenols has been recognized by domestic and foreign researchers, and also become a hot research. The antitumor effect and mechanism of tea polyphenols are constantly clear. Studies have shown that in animal models, EGCG in vivo and in vitro inhibit tumor cell proliferation and apoptosis through a variety of signaling pathways. EGCG inhibits not only the incidence of various cancer but also can reduce the formed tumor size, number and invasion and metastasis.[Objectives] To construct a colon cancer model of Sprague-Dawley(S-D) rats. And to observe the inhibition effects of different doses of EGCG on the growth of colon cancer.[Methods] Colon cancer was induced consistently in experimental wistar rats by carcinogen DMH. Fifty rats were randomly divided into five groups and ten of each: (1)Model group (2)Control group (3)EGCG low dose group (4)EGCG medium dose group (5)EGCG high dose group. All the groups received s.c. DMH at the dose of 30mg/kg body weight twice weekly for 8 weeks except control group. EGCG low dose group received 50mg/kg/d, EGCG middle-dose group received 100mg/kg/d, EGCG high-dose group received 200mg/kg/d everyday for 8 weeks. The control group received equal volume of NS.All the rats were executed after 12 weeks and 20 weeks.[Results]1. Before the experiment, rats weight of control group,model group,EGCG low, medium and high group were (174.5±6.2)g, (176.6±4.8)g, (174.2±5.7)g, (174.6±5.2)g, and there was no significant difference between the groups.From the third week, High-dose treatment group compared with the control group significantly reduced weight. At the end of the experiment, rats weight of control group, model group, EGCG low, medium and high-dose group were (216.1±8.6)g, (221.7±7.3)g, (218.4±7.01)g, (211.8±3.6)g, and there were significantly differences between model group and EGCG high-dose group (P<0.05).2. Except the control group, the other groups were given DMH for 20 weeks, and the average ACF of intestinal mucosa with model group, EGCG low, medium and high-dose group were 5.0±2.0,4.9±2.8,3.9±1.5,3.9±1.5. But there were no significant differences among all groups (P>0.05). The average ACF of colorectal mucosa with model group and EGCG low, medium and high-dose group were 2.8±0.9, 1.8±1.0,1.6±0.5,1.1±0.3, and there were significantly differences between every EGCG groups and model group (P<0.05).3. In the first 12 weeks after modeling, the first rats were killed,5 rats in the model group had all chronic intestinal inflammation; 2 rats of them had colorectal chronic inflammation, and other 2 of 5 showed moderate to severe dysplasia in colorectal. In EGCG low-dose group, there were 4 of 5 rats had chronic inflammation in the small intestine, and the last 1 showed moderate to severe dysplasia in small intestine; 2 rats of them showed chronic inflammation of colorectal, and one of them had moderate to severe dysplasia in colorectal. In EGCG medium-dose group, a total of 4 rats had chronic inflammation in the small intestine; 2 rats showed a chronic inflammation in colorectal, and the other 2 showed moderater to severe dysplasia of colorectal. In EGCG high-dose group, a total of 4 rats showed chronic inflammation in the small intestine; 2 of them had chronic inflammation in colorectal, and the last 2 showed moderate to severe dysplasia. The control group was not any abnormalities. There was no difference among any group in cancer, chronic inflammation and dysplasia of small intestine and colorectal (P>0.05).4. In the 20 weeks after modeling, the second rats were killed.4 of 5 rats in the model group had chronic intestinal inflammation, and 1 of 5 having cancer showed signet-ring cell carcinoma; All 5 rats had colorectal chronic inflammation. In EGCG low-dose group, the total of 5 rats had chronic inflammation in the small intestine and in colorectal. In EGCG medium-dose group, all the 4 rats had chronic inflammation in the small intestine; 1 rat showed chronic inflammation in colorectal, and the other 3 rats showed moderater to severe dysplasia. In EGCG high-dose group,4 of 5 rats showed chronic inflammation in the small intestine, and another one had signet-ring cell carcinoma; 2 of them had moderater to severe dysplasia in colorectal, and the last 3 showed signet-ring cell carcinoma. The contrl group was not any abnormalities. There was no difference among any group in cancer, chronic inflammation and dysplasia of small intestine and colorectal (P>0.05).[Conclusion] (1) DMH can induce the occurrence of colon cancer in rats, EGCG high-dose group can inhibit colon cancer induced by DMH; (2) The formation of ACF in rats significantly reduced by different doses of EGCG.