- 學位論文
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
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。
並列摘要
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.