| Summary: | 碩士 === 國立臺灣大學 === 食品科技研究所 === 96 === Malignant neoplasm is the first cause of ten leading causes of death in 2007 in Taiwan and colorectal cancer is the third cause of cancer death in Taiwan. Epidemiological studies have indicated that colorectal cancer is strongly associated with diet, and thus the occurrence of colorectal cancer may be prevented by dietary modification. Adlay (Coix lachryma-jobi L. var. ma-yuen Stapf) is a grass crop used in traditional Chinese medicine and as a nutritious food. It has been reported that adlay pocesses anti-inflammatory and anti-tumor activity. In animal model, recent studies have shown that diet substituted with 20% dehulled adlay, 1.6% adlay bran and 0.29% ethanolic extract of adlay bran can significantly suppress the formation of preneoplastic lesions (aberrant crypt foci, ACF) in colon carcinogenesis. In addition, ethyl acetate fraction of adlay bran methanolic extract exhibited the growth-inhibiting effect on HT-29 human colon cancer cells. The purpose of this study was to investigate the effect of different levels of ethyl acetate fraction of adlay bran ethanolic extract (ABE-Ea) on colon carcinogenesis in animal model and to investigate whether ABE-Ea could affect colon carcinogenesis through modulation of inflammation-related proteins. Male F344 rats consumed different samples (blank: 0.5 ml water/day, negative control: 0.5% carboxymethyl cellulose /day, positive control: 1.50 mg piroxicam/day, low level of ABE-Ea: 8.64 mg ABE-Ea/day, medium level of ABE-Ea: 17.28 mg ABE-Ea/day, high level of ABE-Ea: 34.56 mg ABE-Ea/day) by tube feeding and received colon-specific carcinogen 1,2-dimethylhydrazin (DMH) by intraperitoneal injection (40 mg/kg body weight, once a week for 4 weeks, blank were received the same dosage of normal saline). After 9 and 18 weeks of induction, rats were sacrificed and colons were removed to examine for ACF, mucin and mucin-depleted foci (MDF, preneoplastic lesions of colon cancer). Colonic mucosa was examined for inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) protein expression. The results indicated that ABE-Ea significantly reduced the numbers of ACF with 1 crypt and inhibited the formation of ACF with 7 and 8 crypts, showing that ABE-Ea could suppress the fission of ACF. ABE-Ea slightly reduced the numbers of ACF in distal colons, significantly suppressed the mucin alteration of ACF and significantly suppressed the COX-2 expression in overall colons, showing that ABE-Ea could delay the colon carcinogenesis by suppressing colonic inflammation. ABE-Ea at the level of 17.28 mg/day exhibited the best preventive effects on colon carcinogenesis as it significantly reduced the number of ACF with 1 crypt, reduced the number of ACF/cm and inhibited the formation of MDF. Results from this study suggest that ABE-Ea reduces different preneoplastic lesions, reduces colonic imflammation and thus delays colon carcinogenesis.
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