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Full list of author information is available at the end of the articleBackground Non-alcoholic fatty liver disease (NAFLD) is a worldwide common liver disease that has an increasing prevalence not only in adults with metabolic syndrome but also in obese children and adolescents [1-3]. Non-alcoholic stea-tohepatitis (NASH) is one of pathologic stages of NAFLD and the main histopathological changes are steatosis, in-flammation and hepatocyte injury with or without fibrosis [4]. Although the precise mechanisms need to be eluci-dated, the two-hit hypothesis of NASH has been widely accepted [5]. The 1st hit involves fat accumulation in the liver as a result of excessive delivery of free fatty acids (FFAs) from the adipose tissue, and imbalance of lipid syn-thesis and export in hepatocyte. The consequent injures such as oxidative stress and inflammation are regarded as the 2nd hit culminating in fibrosis of liver