Galangin modulated oleic acid-induced lipid accumulation in hepatocytes

碩士 === 長庚科技大學 === 健康產業科技研究所 === 107 === Alpinia officinarum Hance (Zingiberaceae) is a common herb in Chinese medicine. The dry rhizome was found that had antibacterial, anti-oxidation, anti-tumor and anti-inflammatory effects. Galangin was isolated from Alpinia officinarum, previously reported that...

Full description

Bibliographic Details
Main Authors: TSAI, YUN-YUN, 蔡昀芸
Other Authors: HUANG, WEN-CHUNG
Format: Others
Language:zh-TW
Published: 2019
Online Access:http://ndltd.ncl.edu.tw/handle/mdv3k3
Description
Summary:碩士 === 長庚科技大學 === 健康產業科技研究所 === 107 === Alpinia officinarum Hance (Zingiberaceae) is a common herb in Chinese medicine. The dry rhizome was found that had antibacterial, anti-oxidation, anti-tumor and anti-inflammatory effects. Galangin was isolated from Alpinia officinarum, previously reported that had anti-inflammatory and anti-tumor effects. However, galangin regulated lipid metabolism in oleic acid induced hepatocytes was elusive. In this study, we will investigate whether galangin can improve oleic acid-induced lipid accumulation in hepatocytes (FL83B cells). FL83B cells treated with 0.5 mM oleic acid for 48 hours to induce as the fatty liver cell model. Then, the cells were treated with various concentrations of galangin for 24 hours. Galangin would increase sterol regulatory element-binding protein 1c and and peroxisome proliferator-activated receptor γ to promoting the expression of fatty acid synthase in FL83B cells. However, galangin could stimulated CPT-1A expression for activated fatty acid β-oxidation, and significantly increased phosphorylation of AMP activated protein kinase (AMPK) to regulate fatty acid synthesis expressions. Taken together, our results suggested that galangin regulated lipid metabolism in fatty liver cells by increasing the β-oxidation of fatty acid metabolism and the activation of AMPK signal pathway. In addition, galangin can also increase the insulin sensitivity of TNF-α-induced insulin resistance.