Non-alcoholic fatty liver disease (NAFLD) is an important chronic liver disease and metabolic syndrome, correlated with diabetes, obesity, and cardiovascular diseases (Angulo, 2002; Marchesini et al., 2003; Yoneda et al., 2012). In recent years, morbidity of NAFLD has grown not only in Eastern but also in Western countries, and high-fat intake has become an important health issue (Kojima et al., 2003; Bhala et al., 2013). A “two-hit” theory is widely advocated to explain the progression of NAFLD although the exact mechanism of NAFLD is still unknown. Lipid deposition in hepatocytes is considered to be the first hit, which caused by insulin resistance and lipometabolism disorder and resulted in non-alcoholic liver simple steatosis (SS). Oxidative stress and the imbalance of proinflammatory cytokines resulting from lipid peroxidation and the increased reactive oxygen species (ROS) are likely to be the second hit. The second hit contributes to the progressive development of non-alcoholic steatohepatitis (NASH), liver fibrosis, cirrhosis, and even hepatocellular carcinoma from SS (Bugianesi et al., 2002). Excessive fatty acids (FA) deposition and its peroxidation in hepatocytes are considered to be the major
