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| 題名: | 米麩油對DMH/DSS誘發鼠大腸癌形成之影響
Effects of rice bran oil on DMH/DSS-induced colon carcinogenesis in rats |
| 作者: | 何佳蓉
Ho Chia-Jung |
| 貢獻者: | 保健營養學研究所
鄭心嫻
施純光 |
| 關鍵詞: | 碩士
指導教授-鄭心嫻
共同指導教授-施純光
委員-江文章
委員-郭靜娟
委員-李信昌
米麩油;異常腺窩病灶;黏液素缺乏病灶;抗氧化;硫巴比妥酸反應物質
Rice bran oil;Aberrant crypt foci;Mucin-depleted foci;Antioxidation;Thiobarbituric acid reactive substances |
| 日期: | 2010 |
| 上傳時間: | 2010-10-21 09:21:08 (UTC+8) |
| 摘要: | 本研究藉由探討化學誘發大腸癌發生之動物模式，探討米麩油對大腸癌形成之影響。F344鼠在整個實驗期皆攝取調整AIN-93G高脂飲食，其中空白組（B組）及負控制組（N組）餵食14%大豆油高脂飲食；正控制組（P組）餵食含0.04% Piroxicam之14%大豆油高脂飲食；低劑量米麩油組（L組）餵食含5%米麩油及9%大豆油高脂飲食；中劑量米麩油組（M組）餵食含9%米麩油及5%大豆油高脂飲食；高劑量米麩油組（H組）餵食含14%米麩油高脂飲食。除了B組外，其餘組別皆以1,2-Dimethylhydrazine/ dextran sulfate sodium （DMH/DSS）誘導結腸發炎相關之大腸癌發展。於實驗期13週後予以犧牲，以DMH/DSS誘發之鼠取其大腸分析異常腺窩病灶（Aberrant crypt foci, ACF）、黏液素分泌型態及黏液素缺乏病灶（Mucin-depleted foci, MDF）。所有組別之鼠取其肝臟及大腸組織分析超氧歧化酶（Superoxide dismutase, SOD）、觸酶（Catalase, CAT）活性、麩胱甘肽（Glutathione, GSH）濃度及硫巴比妥酸反應物質（Thiobarbituric acid reactive substances, TBARS）濃度。結果顯示，不同劑量米麩油皆可顯著減少總ACF數、總異常腺窩（Aberrant crypt, AC）數，以及小型及大型ACF數。此外，不同劑量米麩油也皆可顯著減少同時分泌Sulfomucin和Sialomucin的ACF（MIX-ACF）數、主要分泌Sialomucin的ACF（SIM-ACF）數，以及MDF與腫瘤數目，而其中以中、高劑量米麩油組的效果較佳。在肝臟抗氧化及脂質過氧化分析結果方面，有誘發的N組與無誘發之B組相較下，其GSH濃度、SOD及CAT活性顯著較低，而TBARS濃度顯著較高。M組及H組其GSH濃度及SOD活性顯著高於N組，H組其CAT活性顯著高於N組，而不同劑量米麩油組其肝臟TBARS濃度皆顯著低於N組。本實驗結果顯示米麩油可增加肝臟抗氧化物質，降低TBARS濃度，進而抑制大腸中ACF形成，改變黏液素分泌形態，以及抑制MDF與腫瘤形成，推測米麩油具有延緩大腸癌進展的潛力。
The purpose of this study was to investigate the effects of rice bran oil on colon carcinogenesis using a chemically induced animal model. F344 rats were fed a modified AIN-93G 14% high-fat diet: groups B and N, 14% soybean oil; group P, 14% soybean oil containing 0.04% piroxicam; group L, 5% rice bran oil and 9% soybean oil; group M, 9% rice bran oil and 5% soybean oil; group H, 14% rice bran oil. All rats except for those in group B were administrated with 1,2-dimethylhydrazine/dextran sulfate sodium (DMH/DSS) to induce colitis-related colon carcinogenesis. After 13 weeks of experimental period, DMH/DSS-treated rats were sacrificed and colons were removed to examine for aberrant crypt foci (ACF), mucin and mucin-depleted foci (MDF). All rats' liver and colon tissues were examined for superoxide dismutase (SOD) activity, catalase (CAT) activity, glutathione (GSH) level and thiobarbituric acid reactive substances (TBARS) level. The results showed that all doses of rice bran oil significantly reduced the numbers of total ACF, total aberrant crypts (AC), small and large ACF. Moreover, all doses of rice bran oil significantly reduced the numbers of ACF producing both sulfomucin and sialomucin (MIX-ACF), ACF producing sialomucin (SIM-ACF), MDF and tumors, especially in group H. Group N had significantly lower hepatic GSH level, SOD and CAT activity, and higher TBARS level than did group B. Groups M and H had significantly higher hepatic GSH level and SOD activity than did group N, and group H had significantly higher hepatic CAT activity than did group N. In addition, all doses of rice bran oil significantly reduced TBARS level as compared to group N. These results indicated that rice bran oil was able to increase hepatic antioxidant-associated parameters and reduced TBARS level, to inhibit colonic ACF formation, to modify mucin composition, and to inhibit MDF and tumor formation, suggesting that rice bran oil has the potential for deferring colon carcinogenesis. |
| 關聯: | 115頁 |
| 描述: | 摘要…………………………………………………………………………………………. Ⅰ
目錄………………………………………………………………………………………..... Ⅴ
表目錄……………………………………………………………………………………..... Ⅷ
圖目錄……………………………………………………………………………………..... Ⅸ
第一章 前言………………………………………………………………………………... 1
第二章 文獻回顧…………………………………………………………………………... 3
2.1大腸癌…………………………………………………………………………………... 3
2.1.1大腸構造與位置…………………………………………………………………….. 3
2.1.2大腸癌形成………………………………………………………………………….. 4
2.1.3大腸癌與飲食……………………………………………………………………….. 6
2.1.4大腸癌與ACF……………………………………………………………………….. 7
2.1.5大腸癌與黏液素…………………………………………………………………….. 10
2.1.6大腸癌與發炎……………………………………………………………………….. 13
2.1.7氧化壓力與抗氧化防禦系統……………………………………………………….. 15
2.1.8大腸癌與iNOS及COX-2………………………………………………………….. 19
2.1.9 DMH/DSS誘發大腸癌機制………………………………………………………... 20
2.2米麩油…………………………………………………………………………………... 23
2.2.1米及米麩簡介……………………………………………………………………….. 23
2.2.2 米麩油簡介………………………………………………………………………..... 26
2.2.3米麩油與疾病……………………………………………………………………….. 27
2.2.4米麩油與大腸癌…………………………………………………………………….. 28
第三章 研究動機…………………………………………………………………………... 31
第四章 材料方法…………………………………………………………………………... 33
4.1實驗材料………………………………………………………………………………... 33
4.1.1實驗動物…………………………………………………………………………….. 33
4.1.2飼料組成…………………………………………………………………………….. 33
4.1.3實驗藥品…………………………………………………………………………….. 33
4.1.4儀器設備…………………………………………………………………………….. 36
4.2實驗方法………………………………………………………………………………... 38
4.2.1米麩來源…………………………………………………………………………….. 38
4.2.2米麩油萃取流程…………………………………………………………………….. 38
4.2.3飼料配製…………………………………………………………………………….. 39
4.2.4實驗動物與飼養…………………………………………………………………….. 42
4.2.5實驗組別架構及流程……………………………………………………………….. 42
4.3分析項目………………………………………………………………………………... 45
4.3.1大腸組織分析……………………………………………………………………….. 45
4.3.1.1 腫瘤分析法……………………………………………………………………… 45
4.3.1.2 ACF 分析………………………………………………………………………... 45
4.3.1.3黏液素分析……………………………………………………………………..... 46
4.3.1.4 COX-2與iNOS蛋白質表現量分析……………………………………………. 47
4.3.2肝臟與大腸組織分析……………………………………………………………….. 48
4.3.2.1 TBARS濃度測定………………………………………………………………... 48
4.3.2.2 SOD活性測定…………………………………………………………………… 49
4.3.2.3 CAT活性測定……………………………………………………………………. 51
4.3.2.4 GSH濃度測定…………………………………………………………………… 53
4.4統計分析………………………………………………………………………………. 54
第五章 結果………………………………………………………………………………... 55
5.1 各組F344鼠攝食及生長狀況………………………………………………………... 55
5.2 米麩油對F344鼠大腸ACF形成之影響…………………………………………… 57
5.3 米麩油對F344鼠遠端大腸黏液素型態之影響……………………………………... 63
5.4 米麩油對F344鼠大腸MDF形成之影響……………………………………………. 67
5.5 米麩油對F344鼠大腸腫瘤形成之影響……………………………………………... 69
5.6 米麩油對F344鼠肝臟及大腸脂質過氧化情形與抗氧化能力之影響…………....... 71
5.7 米麩油對F344鼠大腸黏膜COX-2與iNOS蛋白質表現量之影響………………… 73
第六章 討論………………………………………………………………………………... 80
6.1 米麩油對F344鼠攝食量及生長狀況………………………………………………... 80
6.2 米麩油對F344鼠大腸早期病變ACF之形成……………………………………...... 81
6.3 米麩油對F344鼠遠端大腸黏液素分泌型態之影響………………………………... 84
6.4 米麩油對F344鼠大腸癌形成之MDF與腫瘤之影響………………………………. 85
6.5米麩油對F344鼠肝臟脂質過氧化與抗氧化能力之影響…………………………… 87
6.6米麩油對F344鼠大腸黏膜COX-2與iNOS蛋白質表現量之影響…………………. 90
第七章 結論………………………………………………………………………………... 94
第八章 參考文獻…………………………………………………………………………... 95
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