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补充紫米提取物的饮食通过抑制细菌β-葡萄糖醛酸酶减少二甲基肼诱导的大鼠结肠异常隐窝病灶。

Purple rice extract supplemented diet reduces DMH- induced aberrant crypt foci in the rat colon by inhibition of bacterial β-glucuronidase.

作者信息

Summart Ratasark, Chewonarin Teera

机构信息

Department of Biochemistry, Faculty of Medicine, Chiangmai University, Chiangmai, Thailand E-mail :

出版信息

Asian Pac J Cancer Prev. 2014;15(2):749-55. doi: 10.7314/apjcp.2014.15.2.749.

Abstract

BACKGROUND

Purple rice has become a natural product of interest which is widely used for health promotion. This study investigated the preventive effect of purple rice extract (PRE) mixed diet on DMH initiation of colon carcinogenesis.

MATERIALS AND METHODS

Rats were fed with PRE mixed diet one week before injection of DMH (40 mg/kg of body weight once a week for 2 weeks). They were killed 12 hrs after a second DMH injection to measure the level of O6-methylguanine and xenobiotic metabolizing enzyme activities.

RESULTS

In rats that received PRE, guanine methylation was reduced in the colonic mucosa, but not in the liver, whereas PRE did not affect xenobiotic conjugation, with reference to glutathione-S-transferase or UDP-glucuronyl transferase. After 5 weeks, rats that received PRE with DMH injection had fewer ACF in the colon than those treated with DMH alone. Interestingly, a PRE mixed diet inhibited the activity of bacterial β-glucuronidase in rat feces, a critical enzyme for free methylazoxymethanol (MAM) release in the rat colon. These results indicated that purple rice extract inhibited β-glucuronidase activity in the colonic lumen, causing a reduction of MAM-induced colonic mucosa DNA methylation, leaded to decelerated formation of aberrant crypt foci in the rat colon.

CONCLUSIONS

The supplemented purple rice extract might thus prevent colon carcinogenesis by the alteration of the colonic environment, and thus could be further developed for neutraceutical products for colon cancer prevention.

摘要

背景

紫米已成为一种备受关注的天然产物,被广泛用于促进健康。本研究调查了紫米提取物(PRE)混合饮食对二甲基肼(DMH)引发结肠癌的预防作用。

材料与方法

在注射DMH(40mg/kg体重,每周一次,共2周)前一周,给大鼠喂食PRE混合饮食。在第二次注射DMH后12小时处死大鼠,以测量O6-甲基鸟嘌呤水平和外源性代谢酶活性。

结果

在接受PRE的大鼠中,结肠黏膜中的鸟嘌呤甲基化减少,但肝脏中未减少,而PRE对谷胱甘肽-S-转移酶或尿苷二磷酸葡萄糖醛酸基转移酶介导的外源性结合无影响。5周后,接受PRE并注射DMH的大鼠结肠中的异常隐窝灶比单独接受DMH治疗的大鼠少。有趣的是,PRE混合饮食抑制了大鼠粪便中细菌β-葡萄糖醛酸酶的活性,该酶是大鼠结肠中游离甲基偶氮甲醇(MAM)释放的关键酶。这些结果表明,紫米提取物抑制了结肠腔内β-葡萄糖醛酸酶的活性,导致MAM诱导的结肠黏膜DNA甲基化减少,从而减缓了大鼠结肠中异常隐窝灶的形成。

结论

补充紫米提取物可能通过改变结肠环境预防结肠癌,因此可进一步开发用于预防结肠癌的营养保健品。

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