Zhang, Hai, Chen, Qingshan, Dahan, Arik, Xue, Jiyang, Wei, Liwen, Tan, Weifeng, and Zhang, Guoqing
Liver fibrosis is a progression of chronic liver disease with lacks effective therapies at present. Schisandrin B (Sch B), a bioactive compound extracted from the traditional Chinese medicine Schisandra chinensis , was reported to benefit liver diseases. This study aimed to investigate the therapeutic effects and molecular mechanisms of Sch B against CCl 4 -induced liver fibrosis in rats. RNA sequencing and transcriptome analysis were performed collaboratively, including analysis of differential gene expression, gene ontology (GO) analysis, pathway analysis and pathway-act-network analysis. The results demonstrated that Sch B effectively alleviated CCl 4 -induced liver damage and fibrosis in rats, as evidenced by improved liver function and decreased extracellular matrix deposition. Furthermore, 4440 (1878 up-regulated, 2562 down-regulated) genes in the model group versus (vs) normal group, 4243 (2584 up-regulated, 1659 down-regulated) genes in Sch B-treated group vs model group were identified as differentially expressed genes (DEGs). Subsequently, GO analysis revealed that DEGs were mainly enriched in metabolism, oxidation-reduction, endoplasmic reticulum stress and apoptosis-related biological processes. Pathway analysis suggested that Sch B up-regulated cytochrome P450 drug metabolism, PPAR signaling pathways, and down-regulated glutathione metabolism pathways. In addition, the regulatory patterns of Sch B on key genes and pathways were also confirmed. In conclusion, our study demonstrated Sch B alleviated CCl 4 -induced liver fibrosis by multiple modulatory mechanisms, which provide new clues for further pharmacological study of Sch B. Image 1 • Schisandrin B (Sch B) effectively ameliorated CCl4-induced liver fibrosis in rats. • Sch B regulated oxidation-reduction, endoplasmic reticulum stress and apoptosis. • CYP450 enzymes and PPAR signaling pathway were the main targets of Sch B. [ABSTRACT FROM AUTHOR]