Plumbagin ameliorates liver fibrosis via a ROS-mediated NF-кB signaling pathway in vitro and in vivo

Abstract Aims The purpose of this study was to investigate plumbagin (PL) on liver fibrosis in vitro and in vivo and to explore the underlying mechanisms. Methods Carbon tetrachloride (CCl 4 ) was used to establish a rat liver fibrosis model, primary hepatic stellate cells (HSCs) were isolated from the rat liver, and fibrosis-related indicators were detected. Results The results revealed that PL significantly prevented CCl 4 -induced liver fibrosis, as evidenced by the attenuation of histopathological changes, the decrease of MDA and the increase of SOD and GSH-P X . In addition, PL downregulated the mRNA levels of NOX4 and procollagen I; the protein expression levels of NOX4 and p-IκB; and the transcriptional activity of NF-κB in liver fibrosis rats. Moreover, PL significantly decreased ROS expression, protein expression of α-SMA and collagen III, and activation of NF-κB and inhibited the nuclear translocation of NF-κB p65 in IL-1β-stimulated HSCs in vitro. Conclusion The results of our study indicate that PL can mitigate liver fibrosis in vitro and in vivo, which may be related to the ROS-mediated NF-кB signaling pathway.