Study of Arctigenin Against Nonalcoholic Fatty Liver Disease

• Main Authors: HSU, REN-YI, 許任儀
• Other Authors: CHEN, YU-PEI
• Format: Others
• Language: zh-TW
• Published: 2016
• Online Access: http://ndltd.ncl.edu.tw/handle/94080179599518681368

碩士 === 中華科技大學 === 健康科技研究所 === 104 === After the control of hepatitis viruses and westernization of the lifestyle in Taiwan, an increasing burden of Nonalcoholic fatty liver disease (NAFLD) is anticipated and active prophylactic measures should be implemented. NAFLD is a clinicopathological term that encompasses a spectrum of abnormalities ranging from simple triglyceride accumulation in the hepatocytes to hepatic steatosis with inflammation, also known as nonalcoholic steatohepatitis (NASH). NASH can also progress to hepatic fibrosis, cirrhosis, and hepatocellular carcinoma. In this study, lipid droplets formation was accumulated by oleic acid (OA) treatment in WRL68 hepatocytes to mimic NAFLD with excessive free fatty acids into hepatocytes. The data demonstrates that arctigenin (ATG) has good beneficial effects to retard NAFLD development. ATG protects WRL68 cells from lipotoxicity to against excessive OA accumulation. Meanwhile, ATG prevented OA mediated lipid droplets accumulation, oxidation stress and inflammation. In addition, the results suggested that ATG induced AKT phosphorylation to sustain cell survival. Activation of AMPK downregulated ACC1 and SREBP-1 expression to reduce fatty acid synthesis, and upregulated PPARα and CPT-1 expression to accelerate lipolysis and ROS remove. Importantly, ATG significantly inhibited elevation of U937 macrophage chemoattractant, ICAM-1, IL-1β, IL-6, IL-6sR, IL-7 and IL-8. Thus, ATG may have potential to improve NAFLD progression.