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研究生: 李翊銘
Lee, Yi-Ming
論文名稱: 冷壓椰子油對葡聚醣硫酸鈉誘導的潰瘍性結腸炎之保護效果
Protective Effect of Cold Pressed Coconut Oil on Dextran Sulfate Sodium-induced Ulcerative Colitis in Rats
指導教授: 劉明毅
Liu, Ming-Yie
學位類別: 碩士
Master
系所名稱: 醫學院 - 環境醫學研究所
Department of Environmental and Occupational Health
論文出版年: 2018
畢業學年度: 106
語文別: 英文
論文頁數: 66
中文關鍵詞: 潰瘍性結腸炎椰子油發炎氧化壓力
外文關鍵詞: Ulcerative colitis, coconut oil, inflammation, oxidative stress
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  • 潰瘍性結腸炎是一種結腸黏膜下層的非特異性發炎疾病,其病徵為腹瀉、腹痛、血便,惡化則會造成大腸癌。椰子油是從椰子果肉內萃取出來的食用油品,其中含有大量容易被動物體吸收的中鏈飽和脂肪酸、酮體以及多酚類,這些內含物皆具有良好的抗發炎與抗菌能力。本研究的目的為探討冷榨椰子油對於葡聚醣硫酸鈉所誘導的急性潰瘍性結腸炎之保護效果。冷榨椰子油製備是取熟成椰子果肉,低溫乾燥後研磨萃取其油脂。實驗以管餵的方式連續十日給予大鼠椰子油(2 ml/kg和4 ml/kg),並將葡聚醣硫酸鈉(3%)添加於大鼠飲用水中連續七日以誘發急性結腸炎,實驗期間每天進行病理活性指標評估,於第11天時犧牲並取其血液及器官做分析。另外,利用腸道表皮細胞(IEC-6)來測試椰子油中所含有的中鏈脂肪酸以及酚類對於細胞活性及氧化壓力的影響。結果顯示,在誘導潰瘍性結腸炎後給予椰子油,可以增加大鼠的攝食量,並同時降低結腸炎的病理活性指標,另外,可以回復大鼠大腸長度與水腫狀況,減少因發炎造成的脾臟腫大情形,減緩在大腸組織內的傷害,且白血球浸潤狀況也有改善,骨髓過氧化酶活性、丙二醛含量與介白質-1β之表現量也有減少的趨勢。餵食椰子油後,黏蛋白-1與酸性黏蛋白的表現量也都有減少,對於動物體內其他器官以及血脂無顯著影響。在細胞實驗中,發現月桂酸、癸酸和辛酸在對於IEC-6細胞不會有保護效果,且在高劑量下具有細胞毒性。多酚類阿魏酸與對香豆酸對於細胞株也減少了其細胞活性。綜合上述結果,雖然椰子油中鏈脂肪酸與多酚類的個別成分具有細胞毒性;在動物試驗中對其他器官無明顯傷害,可經由降低氧化壓力與發炎反應以達到保護DSS所誘導之潰瘍性結腸炎的效果。

    Ulcerative colitis (UC) is an inflammatory bowel disease which may lead to diarrhea, abdominal pain, rectal bleeding, and colorectal cancer. Coconut oil (CO) is an edible oil extracted from the kernel of a mature coconut. It contains medium-chain fatty acids and phenols, both of which are easily absorbed and possess antimicrobial and anti-oxidant capabilities. However, the protective effect of CO on UC has never been studied. Therefore, the aim of this study was to investigate the protective effect of cold pressed unprocessed CO against UC in rats. CO (2 ml and 4 ml/kg rat) was gavaged to Wistar rats once a day for 10 days. UC was induced by administrating 3% dextran sulfate sodium (DSS) in drinking water on the 3rd day for 7 days and disease activity index (DAI) was monitored. Blood and organs were collected on the last day for analysis. In the UC rats, CO decreased DAI score and increased food intake and it also restored colon length, and decreased colon edema and spleen weight. CO attenuated submucosal ulceration, edema, crypt damages and leukocyte infiltration while decreasing myeloperoxidase activity, malondialdehyde level, caspase-1 and IL-1β expression in the DSS-induced UC. Acidic mucin and mucin-1 production in colitis were also decreased as a result of CO feeding in DSS-induced UC rats. No adverse effect of coconut oil on other organs and blood lipid profile was observed between control groups. However, medium-chain fatty acids and polyphenols decreased cell viability in IEC-6 at tested concentrations. In conclusion, coconut oil attenuates DSS-induced ulcerative colitis by decreasing oxidative stress and inflammation in the colon thereby protecting rats from UC without observed changes in other organs.

    Content 摘要 I Abstract II Acknowledgement III Content V Figure contents VI 1. Introduction 1 2. Objective 7 3. Materials and methods 8 4. Results 20 5. Discussion 26 6. Conclusion 32 7. Reference 33 8. Figures 40

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