Desferal (Deferoxamine) Targets Ferroptosis Triggered by Chrysophanol in Hepatic B Virus X Protein-Induced Hepatic Stellate Cell Activation

Abstract

Iron plays a key role in the regulation of hepatic stellate cell activation during the pathogenesis of liver fibrosis. Prevention of hepatic stellate cell activation and promotion by activating hepatic stellate cells to death is a good strategy for resolution of liver fibrosis. Ferroptosis is an iron dependent cell death, which is characterized by accumulation of lipid peroxides. We have shown in our earlier studies that chrysophanol (isolated from Rheum palmatum rhizomes) promotes (hepatitis B virus X protein)-activated hepatic stellate cells to ferroptosis; however, the effect of desferal in our cell model is still unclear. In this study, we have shown that desferal reversed chrysophanol-induced lipid reactive oxygen species overproduction and cell death in (hepatitis B virus X protein)-activated T6 cells. Furthermore, desferal also alleviated and chrysophanol downregulated the expressions of á-smooth muscle actin, connective tissue growth fac, glutathione peroxidase 4, and solute carrier family 7-member 11 protein in hepatitis B virus X protein-activated T6 cells. In conclusion, desferal regulates ferroptosis induced by chrysophanol in hepatitis B virus X protein-activated hepatic stellate cell activation and fibrosis.