表没食子儿茶素没食子酸酯对炎症性肠病大鼠肠黏膜的保护作用  

Protective effect of epigallocatechin-3 -gallate on inflammatory bowel disease:experiment with rat models of induced colitis

作　　者：林英卓[1] 陈烨[1] 宋于刚[1] 

机构地区：[1]南方医科大学南方医院消化内科研究所,广州510515

出　　处：《中华医学杂志》2007年第42期2965-2968,共4页National Medical Journal of China

摘　　要：目的探索儿茶素单体表没食子儿茶素没食子酸酯(EGCG)对炎症性肠病(IBD)模型大鼠肠黏膜的保护作用及机制。方法将72只健康 SD 大鼠随机分为正常对照组,模型组,药物阳性对照组,大、小剂量(100、50 mg/kg)EGCG 组及 EGCG 预处理组,每组12只,以三硝基苯磺酸(TNBS)灌肠制作大鼠 IBD 模型。灌肠用药2周后,评价各组大鼠肠黏膜病理组织学表现及评分;应用免疫组织化学法和半定量逆转录(RT)-PCR 法分别从蛋白、mRNA 水平检测各组肠黏膜细胞环氧合酶(COX)-2表达水平的变化。结果不同剂量 EGCG 灌肠均能不同程度改善 IBD 模型大鼠肠黏膜病理组织学征象,其中模型组,EGCG 大、小剂量组组织学评分为6.8±1.0、3.6±0.8、4.1±1.0,后两者与模型组相比差异均有统计学意义(均 P<0.05),均能抑制肠黏膜细胞 COX-2的蛋白和 RNA表达水平,且与用药剂量呈一定量效关系;其中以 EGCG 预处理组的效果最好(P<0.01)。结论EGCG 对 IBD 模型大鼠肠黏膜有保护作用,该作用可能是通过抑制 COX-2的活性实现。Objective To explore the protective effect of epigallocatechin-3-gallate （EGCG） on ulcerative colitis （UC） and mechanism thereof. Methods Sixty SD rats underwent enema of trinitrobenzene sulfonic acid （TNBS） to cause UC and then randomly divided into 6 groups： model group, undergoing enema of normal saline （NS） once a day for 2 weeks; positive drug control group, undergoing enema of 5- aminosalicylic acid （ASA）, an anti-UC drug; high-dose EGCG group, undergoing enema of 100 mg/kg EGCG; low-dose EGCG group, undergoing 5enema of 50 mg/kg EGCG; and EGCG pretreatment group, undergoing enema of 100 mg/kg once a day 3 days before the model establishment and then once a day for 2 weeks after the model establishment. Another 12 rats were used as normal controls. Two weeks later the rats were killed. The histological score of the colonic mucosa was evaluated. The cyclooxygenase-2 protein expression in the colonic mucosa was detected by immunohistochemistry and the cyclooxygenase-2 mRNA expression was assessed by semiquantitative reverse-transcription polymerase chain reaction. Results The histological score of the model group was 6.4 ± 2.7, significantly higher than that of the normal control group （ 1.0 ± 0.7, P 〈 0.01 ）. The histological scores of the 5-ASA, and 100 mg/kg and 50 mg/kg EGCG groups were 3.4 ±1.8, 2.6 ± 1.5, and 4.0 ± 2.0 respectively, all significantly lower than that of the model group （ all P 〈 0.05 ）. The histological scores of the EGCG pretreatment group was the lowest （ 1.2 ±0.8 ）, especially compared with the model group （P 〈0.01 ）. Cyclooxygenase -2 mRNA was not expressed in the normal control group, was highly expressed in the model group, and the expression levels of the 5-ASA and EGCG groups were all significantly lower than that of the model group （ X^2 = 22. 017, P 〈 0. 05 ）. Conclusion Preventing and ameliorating colitis by inhibiting cyclooxygenase-2 activity, EGCG may be a potential medicine in treating inflammatory bowel disease.

关 键 词：结肠炎 环氧化合物 大鼠 表没食子儿茶素没食子酸酯 

分 类 号：R574.6[医药卫生—消化系统]