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张萍, 李百祥, 高淑英. 熊脱氧胆酸对小鼠结肠癌抑制作用及机制[J]. 中国公共卫生, 2008, 24(12): 1487-1488. DOI: 10.11847/zgggws2008-24-12-39
引用本文: 张萍, 李百祥, 高淑英. 熊脱氧胆酸对小鼠结肠癌抑制作用及机制[J]. 中国公共卫生, 2008, 24(12): 1487-1488. DOI: 10.11847/zgggws2008-24-12-39
ZHANG Ping, LI Bai-xiang, GAO Shu-ying. Inhibition effect of ursodeoxycholic acid on colon cancer in 1, 2-dimethylhydrazine-treated ICR mice[J]. Chinese Journal of Public Health, 2008, 24(12): 1487-1488. DOI: 10.11847/zgggws2008-24-12-39
Citation: ZHANG Ping, LI Bai-xiang, GAO Shu-ying. Inhibition effect of ursodeoxycholic acid on colon cancer in 1, 2-dimethylhydrazine-treated ICR mice[J]. Chinese Journal of Public Health, 2008, 24(12): 1487-1488. DOI: 10.11847/zgggws2008-24-12-39

熊脱氧胆酸对小鼠结肠癌抑制作用及机制

Inhibition effect of ursodeoxycholic acid on colon cancer in 1, 2-dimethylhydrazine-treated ICR mice

  • 摘要: 目的 探讨熊脱氧胆酸(UDCA)对1,2-二甲肼(DMH)所致小鼠结肠癌抑制作用及可能机制.方法 ICR小鼠喂养1周后,按体重随机分为3组,其中2组腹腔注射DMH,剂量30mg/(kg.bw),每周1次,连续6周诱导结肠癌模型,另一组为空白对照组.从第7周开始在一组(UDCA组)饲料中添加UDCA,剂量3g/kg;另一组(DMH组)饮食不做处理.所有各组均喂食标准AIN-93饲料,28周后处死小鼠,取结肠粘膜进行小鼠碱性鞘磷脂酶(alk-SMase)的活性表达分析.结果 与DMH组相比,给予UDCA组小鼠结肠肿瘤数目明显减少(t=2.77,P<0.05),病理检查肿瘤恶性程度也显著低于DMH组;alk-SMase活性检测中,UDCA组结肠粘膜及内容物alk-SMase活性分别为22.56%和28.97%,其中结肠内容物活性UDCA组比DMH组提高了近14倍;蛋白免疫印迹试验时,UDCA组alk-SMase蛋白表达明显强于DMH组.结论 UDCA对DMH所致小鼠结肠癌有抑制作用,其可能的机制是通过上调小鼠结肠粘膜alk-SMase活性及表达.

     

    Abstract: Objective To investig ate the inhibition effect of ursodeox ycholic acid(UDCA)on colon cancer and its potential mechanism in 1,2-dimethylhy drazine-treated ICR mice.Methods After acclimation for 1 week,ICR mice were randomly divided into three groups according to weight.One group was blank control and the mice of other two g roups were injectedi.p.with DMH(30 mg/kg穊w)in 1mmo l/LEDTA once a week fo r 6 weeks.One group was UDCA group fed with AIN-93 diet with UDCA(3g/kg)from the 7th week.The other group(DMH group)and control group mice were fed with AIN-93 diet.A fter 28 weeks,all mice were killed.The mucous membrane of colon was obtained and the activity and expression of alk-SM ase were analyzed.Results Compared with DMH group,the number and malig nant degree of colon tumors in UDCA group was significantly decr eased(t=2.77,P<0.05).F urthermore,the alk-SM ase activity of UDCA group in colon mucosa and content was 22.56% and 28.97% respectively.The activity of colon content increased about 14 times and the expressio n of alk-SM ase was significantly increased in UDCA group compared with DMH g roup.Conclusion Long-term administration of UDCA could inhibit the carcinogenesis of colon cancer in DMH-treated ICR mice and the potential mechanism of UDCA chemoprev ention of colon cancer is regulating up the activity and expression of alk-SM ase.

     

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