The rat lncRNA and mRNA microarray analysis of the 6 samples from2-AAF/PH group and Diwu Yanggan capsule treatment group

In some previous studies, DWYG played key roles in improving immune-modulatory responses, ameliorating liver lesions, enhancing liver regeneration, virus-killing activities and HCC inhibition. It has been shown that liver injury caused by an array of factors, can significantly hinder the regenerative effects of mature hepatocytes on liver parenchyma. However, factors such as 2-acetylaminofluorene (2-AAF) induce hepatocyte injury to limit the regenerative ability of liver. In addition, 2-AAF exposure results in cell lysis and disrupts other liver functions. These have made the 2-AAF/PH animal model the most commonly used in assessing the mechanisms by which medicines exert therapeutic effects. In our previous study, it has been demonstrated that DWYG could control HCC in 2-AAF/PH rats, potentially through the modulation and restoration of the liver regeneration microenvironment.However, the comprehensive mechanisms of 2-AAF/PH-induced rat pathogenesis and the pharmacological mechanisms of DWYG is still poorly understood. The present study there aims to explore the mechanisms by which DWYG regulates hepatic transcriptome in a 2-AAF/PH-induced rat model in view of enhancing its applications in liver treatment. Specific-pathogen-free (SPF) male Wistar rats (180 ± 10 g) were kept under controlled environmental conditions at 21 ± 2 °C and with a 12-h light/dark cycle and fed drinking water and pellet food ad libitum. For the model and DWYG groups, the rats received partial hepatectomy and then orally administered 20 mg/kg 2-AAF once a day for one week. The rats of the DWYG group were orally administrated 10 mL/kg until sacrificed. On the last day of study, the mice were sacrificed under humane conditions, the liver tissues were then collected and stored at −80 °C for microarray data analysis.