Abstract
Fuzheng huayu formula (FZHY), an antifibrotic traditional Chinese medicine, is frequently used for the treatment of liver fibrosis. In this study, network analysis, transcriptomic analysis, assays of cell apoptosis, viability and protein expression were used for investigating the effects and mechanisms of compounds derived from FZHY on hepatic parenchymal cell (HPC) protection and hepatic stellate cell activation. Network pharmacology analysis found that 6 major compounds and 39 potential targets were important network nodes. Our analysis predicted that the active compounds of FZHY, including hederagenin, luteolin and tanshinone IIA inhibited cell apoptosis (p < 0.05), increased PI3K expression and reduced cleaved caspase 3 expression and the Bax/Bcl-w ratio (p < 0.05) in L02 cells that had apoptosis induced by TNF-α. Few significant changes caused by FZHY, hederagenin, luteolin and tanshinone IIA were observed in hepatic stellate Lx2 cells upon TGF-β1 induction. These data suggest that FZHY is active against liver fibrosis, protects hepatic parenchymal cells from apoptosis, and recovers liver function, possibly through the effects of its active compounds hederagenin, luteolin and tanshinone IIA and is involved in the inhibition of apoptosis in HPCs, possibly through regulating the PI3K, ERK, cleaved caspase 3 and Bax/Bcl-w levels.
Highlights
Liver fibrosis, characterized by fibrosis and the accumulation of collagen [1,2], is a consequence of liver damage from various sources, including metabolic disorders, hepatic parenchymal cell (HPC)damage, autoimmune diseases, alcohol abuse and hepatic viral infection [3]
A Venn analysis of the genes directly related to Differentially Expressed Genes (DEGs) and targets of FZHY was performed to obtain potential targets of FZHY that may contribute to an anti-fibrotic effect
Liver fibrosis resulting from chronic liver injury is a major causes of morbidity and mortality worldwide [18]
Summary
Liver fibrosis, characterized by fibrosis and the accumulation of collagen [1,2], is a consequence of liver damage from various sources, including metabolic disorders, hepatic parenchymal cell (HPC)damage, autoimmune diseases, alcohol abuse and hepatic viral infection [3]. Liver fibrosis, characterized by fibrosis and the accumulation of collagen [1,2], is a consequence of liver damage from various sources, including metabolic disorders, hepatic parenchymal cell (HPC). Anti-liver fibrosis capability is vital to the study of cirrhosis treatment. The clinical treatment for liver fibrosis has mainly addressed hepatic stellate cell (HSC) activation, apoptosis protection in HPCs, Molecules 2019, 24, 338; doi:10.3390/molecules24020338 www.mdpi.com/journal/molecules. As the foundation of liver function, HPCs make up 70–85% of the liver’s mass. They are involved in protein synthesis, protein storage, transformation of carbohydrates, etc. Damage of HPCs is the necessary prerequisite of liver fibrosis. HPCs apoptosis plays a role in the process of liver fibrosis
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