根據行政院衛生署資料統計在民國八十一年每十萬人口就有18.15的人因慢性肝病及肝硬化的死亡率；而到民國九十三年更上升到23.63的死亡率。然而造成肝硬化的原因有很多，但在西方國家以酒精誘發肝損傷的機率則佔60?70%；酒精誘發肝臟損傷的致病機轉是至今仍未完全清楚。 本實驗模式在酒精誘發肝臟損傷，探討肝臟在給予酒精時的脂質代謝作用是否改變，實驗中利用western blot看蛋白質的表現；另一方面測其氧化壓力下肝臟損害的程度，加入具抗氧化性的厚朴酚或阿魏酸之後，組織形態的改變及組織受損的程度並測量自由基，以達到保護肝臟的功效。 其結果發現在血清中的GOT/GPT，厚朴酚組(97.45±3.88/80.82±6.17)、阿魏酸組(405.4±69.7/140.56±27.1)均比酒精組(817.2±133.7/321.3±196.5)能抑制GOT/GPT上升、並減少肝臟細胞受損。而厚朴酚組跟阿魏酸組降低Leptin的表現量。其Acrp 30、Resistin表現量在酒精組比控制組來的高，而加入阿魏酸發現resistin明顯下降的趨勢、Acrp 30在厚朴酚組、阿魏酸組、Vit E各組均有顯著的被抑制情形。 在細胞凋亡方面，厚朴酚組、Vit E組可以降低經酒精誘發肝臟疾病的細胞凋亡現象，並在肝臟組織內有修復蛋白質增加的表現。 這些結果可使日常生活中多一項保健食品，並降低因酒精所帶來的疾病。; Although alcoholic liver disease (ALD) is recognized as a worldwide major health problem but the pathogenetic mechanisms are still poorly understood. T The purpose of the present study was to evaluate the effect of leptin, resistin and adiponectin in alcohol induced liver damage. On the other hand measure the degree that it oxidizes the pressure to descend the liver damage, after joining the magnolol and the Ferulic acid that the anti- oxidizes, organize the change of the appearance and organize the damaged degree to also measure the free radicals, to reach the effect of protecting the liver. Our result discovered can cause in the blood serum in magnolol and Ferulic acid GOT/GPT to reduce and suppresses Leptin, resistin, the adiponectin expression. The reduction because alcohol causes the situation which the liver cell apoptosis. These results may cause in the daily life more than a health foods, and reduces the disease which because the alcohol brings.
