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

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 (CCl4) 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 CCl4 -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-I kappa B; and the transcriptional activity of NF-kappa B in liver fibrosis rats. Moreover, PL significantly decreased ROS expression, protein expression of alpha-SMA and collagen III, and activation of NF-kappa B and inhibited the nuclear translocation of NF-kappa B p65 in IL-1 beta-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-kappa B signaling pathway.