Expression data from liver of Cyclocarya paliurus triterpenic acids treated high-fat-diet-induced mice

Diverse targets and metabolic pathways are involved in NAFLD, which accounts for the difficulties in achieving the predominant therapeutic effects in clinical practice. Lipid accumulation is the ‘first hit’ in the development of NAFLD in liver, the dysregulation of lipid disposal can lead to hepatic steatosis. Oxidative stress is the ‘second hit’ in the pathogenesis of NAFLD. CP triterpenic acid (CPT) had an ameliorative effect on metabolic diseases, such as non-alcoholic hepatic steatosis. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. Mice were randomly distributed into three groups (n = 5 per group) and were fed with a standard chow diet (normal control group, NC group), an high fat diet [bile sodium 0.5%, cholesterol 2%, yolk 10%, lard 10%, standard diet 77.5% (w/w), about 4016 kcal/kg, 30% of calories from fat] (HFD group), or orally administrated with CPT (160 mg/kg) daily for 8 weeksafter 12 weeks of HFD feeding (CPT group). Mice were anesthetized by 10% chloral hydrate and sacrificed after starving for 12 h at the end of the experiments (0.3 ml/100g body weight). Liver samples were collected and frozen at -80 °C for later analysis.