EGCG促进AOM/DSS诱导小鼠结直肠腺瘤生成

EGCG Promotes the Production of Colorectal Adenoma Induced by AOM/DSS in Mice

目的研究表没食子儿茶素没食子酸酯(EGCG)对氧化偶氮甲烷(AOM)/葡聚糖硫酸钠(DSS)诱导小鼠结直肠腺瘤的影响。方法将30只雌性幼鼠随机分为对照组、AOM/DSS组和AOM/DSS+EGCG组,每组10只。饲养过程中每周观察各组小鼠体质量、精神状态以及排便情况,13周后处死小鼠,观察每组小鼠结直肠腺瘤发生率和肿瘤数量。采用免疫组化方法检测小鼠结直肠肿瘤组织中CD31及CD68的表达情况。结果对照组小鼠无结直肠腺瘤发生,AOM/DSS组和AOM/DSS+EGCG组各有4只小鼠出现结直肠腺瘤,癌变率分别为50.00%(5/10)和66.67%(6/9)(P> 0.05)。在成瘤小鼠肿瘤数量上,AOM/DSS+EGCG组(8.25±2.06)高于AOM/DSS组(3.75±1.71)(P <0.05)。AOM/DSS+EGCG组小鼠结直肠腺瘤组织中CD31和CD68的表达较AOM/DSS组高(P <0.05)。结论 EGCG可能是结直肠非典型增生和结直肠腺瘤发生发展的一个促进因素。

Objective To study the effect of epigallocatechin gallate( EGCG) on colorectal adenoma induced by azoxymethane( AOM)/ dextran sulfate sodium( DSS) in mice. Methods Thirty young,female mice were randomly divided into control,AOM/DSS,and AOM/ DSS+EGCG groups( n = 10 in each group). The body weight,mental status,and defecation of mice in each group was recorded every week,for 13 weeks,at the end of which the mice were sacrificed. The incidence of colorectal adenoma and the number of tumors in each group was recorded. Immunohistochemistry was used to detect the expressions of CD31 and CD68 in colorectal tumor tissues. Results No colorectal adenoma was found in mice of the control group. Colorectal adenoma was found in 4 mice of both AOM/DSS and AOM/DSS+EGCG groups. The incidence of colorectal adenoma was 50.00%( 5/10) in the AOM/DSS group and 66.67%( 6/9) in the AOM/DSS+EGCG group( P > 0.05). The number of tumors in the AOM/DSS+EGCG group was higher than that in the AOM/DSS group (8.25±2.06 vs 3.75±1.71,P < 0.05). The expression levels of CD31 and CD68 in the AOM/DSS+EGCG group were higher than those in the AOM/DSS group( P < 0.05). Conclusion EGCG might promote the occurrence of colon dysplasia and colon adenoma.