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  • 學位論文

沒食子酸經由降低肝臟脂質生成及氧化壓力抑制酒精誘導之脂肪肝炎

Gallic acid inhibits alcohol-induced steatohepatitis via reducing hepatic lipogenesis and oxidative stress in C57BL/6J mice

指導教授 : 王朝鐘

摘要


長期過量飲用酒精會造成酒精性肝病(alcoholic liver disease,ALD),當酒精進入細胞後會經由乙醇脫氫酶催化形成具毒性的乙醛(acetaldehyde),進而產生氧化壓力、脂肪變性、發炎反應,對肝臟造成傷害。沒食子酸(gallic acid,GA)是茶葉中主要的植物酚酸,文獻證實具有抗致突變、抗發炎、抗癌等功效,過去本實驗室證明沒食子酸具抑制發炎反應、增加抗氧化酵素表現量的功能,但影響慢性酒精性肝炎相關的作用機制則需要更進一步的探討。本研究利用C57BL/6 (B6)小鼠觀察沒食子酸是否能有效改善慢性酒精誘導所產生的肝損傷。結果顯示沒食子酸降低血清中GOT、GPT、三酸甘油酯以及膽固醇,減緩酒精對肝臟的傷害;此外也增加抗氧化酵素的活性,抑制酒精對肝臟所造成的氧化作用及發炎反應。根據以上實驗結果,長期的酒精誘導下,沒食子酸具有增加抗氧化酵素的活性、降低發炎反應與氧化作用的能力,達到保護肝臟的目的,希冀將來能有機會發展為治療酒精性肝病之藥物,或者開發為護肝之保健產品。

並列摘要


Long-term excessive drinking alcohol could cause alcoholic liver disease (ALD), ethanol is oxidized to toxic acetaldehyde by dehydrogenase after enter the cell, the production of oxidative stress and the accumulation of steatosis, which induced liver damage. Gallic acid (GA) is the main polyphenolic acid in tea, the literature confirmed with anti-mutagenic, anti-inflammatory, anti-cancer and other effects, the past proved that GA inhibition of inflammation, oxidative enzyme expression, but the impact of chronic alcoholic hepatitis-related mechanisms of action need to be further explored. In this study, C57BL/6 (B6) mice were used to observe whether GA could effectively improve liver injury induced by chronic alcohol. The results showed that GA decreased serum GOT, GPT, triglyceride and cholesterol, reducing alcoholic damage to the liver; in addition to increase the activity of antioxidant enzymes, inhibition of alcohol on the liver caused by oxidation and inflammation. According to the above experimental results showed that GA has increased antioxidant enzyme activity, reduce the ability of inflammation and oxidation, to protect the liver, hoping to have the opportunity to develop the health food for the treatment of alcoholic liver disease, or the health care products for the liver.

參考文獻


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