- 學位論文
龍眼花水萃物對 HepG2 細胞脂質堆積能力之影響
The Effect of Longan Flower Water Extract on Lipid Accumulation in HepG2 cells
摘要
非酒精性脂肪肝是指肝臟的脂質代謝異常，肝臟細胞堆積了過多的脂肪而導致。由於國人的飲食習慣改變，容易從生活中攝取大量的脂肪，導致非酒精性脂肪肝的盛行率有逐年上升的趨勢。龍眼是台灣常見的植物，其花與果實經脫水和烘焙等過程後皆可製成具有經濟價值之產品。龍眼花富含大量的酚類以及黃酮類化合物，具有抗氧化、降低血脂和改善胰島素阻抗之效果。本實驗使用 HepG2 細胞，探討龍眼花水萃物對於肝細胞脂質堆積之影響與可能之機制。本實驗先將細胞處理不同時間之 500 μg/mL龍眼花水萃物，發現處理龍眼花水萃物4小時以上可顯著降低油酸所誘導細胞內三酸甘油酯之堆積。接著以不同濃度的龍眼花水萃物處理細胞 4 小時後，發現 250 μg/mL 以上之龍眼花水萃物即可顯著降低油酸誘發的三酸甘油酯堆積，但在膽固醇堆積上則無效用。實驗進一步探討龍眼花水萃物之可能作用機制，發現其可增加腺苷單磷酸活化蛋白質激酶 (adenosine monophosphate-activated protein kinase, AMPK) 表現量及乙醯輔酶 A 羧化酶 (acetyl-CoA carboxylase, ACC) 的磷酸化能力來抑制細胞內脂質的合成，並可降低固醇調節元件結合蛋白-1 (sterol regulatory element binding protein-1, SREBP-1) 轉運到細胞核內。此外，龍眼花水萃物亦可活化過氧化物酶體增殖物激活受-γ (peroxisome proliferator activated receptor-γ , PPARγ) 轉位至細胞核的能力而達促進脂肪的氧化分解之效果。以上結果證實龍眼花水萃物可減少 HepG2 細胞的脂質堆積，具改善非酒精性脂肪肝之潛力。
並列摘要
Non-alcoholic fatty liver disease (NAFLD) is caused by the hepatic steatosis that lead excessive lipid accumulated in hepatocytes. In recent years, the prevalence of NAFLD was increased gradually due to the dietary habits which make people intake excessive fat from food. Longan is a common plant in Taiwan, its flower and fruit is the value products after dehydrated and roasted process. Longan flower is rich in polyphenols and flavonoids that possessed the improving effect on oxidative stress, hyperlipidemia, and insulin resistance. In this study we investigated the effect of longan flower water extract (LFWE) on lipid accumulation and possible mechanisms in HepG2 cells. First we assessed the time and dose effects of LFWE on oleic acid induced lipid accumulation. However, LFWE had no effect on cholesterol accumulation. The result showed that treated with 250 μg/mL LFWE for 4 hours could significantly reduce intracellular triglyceride accumulation in HepG2 cells. We further investigated the possible mechanism, the data showed that LFWE could increase the total content of adenosine monophosphate-activated protein kinase (AMPK) and phosphorylation level of acetyl-CoA carboxylase (ACC) and decrease translocation of sterol regulatory element binding protein-1 (SREBP-1) to reduce the lipid synthesis in HepG2 cells. Moreover, LFWE could also increase the translocation of peroxisome proliferator activated receptor-γ (PPARγ) from cytosol to nuclear to stimulate the fatty acid oxidation. According to these data, we suggested the LFWE might prevent the NAFLD.