Bile acids inhibit ferroptosis sensitivity through activating farnesoid X receptor in gastric cancer cells

Figure 4 Farnesoid X receptor significantly promoted the synthesis of glutathione and the level of glutathione peroxidase 4 in gastric cancer cells. A-D: Alterations of glutathione (GSH) concentrations and the GSH/oxidized GSH (GSSG) ratio in HGC-27 and MKN-45 cells transfected with the shNC or shFXR plasmid; E and F: Protein expression of GCLC, GSS, GCLM, and GSH peroxidase 4 (GPX4) in HGC-27 and MKN-45 cells transfected with the shNC or shFXR plasmid; G-J: Alterations of GSH concentrations and the GSH/GSSG ratio in HGC-27 and MKN-45 cells transfected with the control or farnesoid X receptor (FXR)-coding plasmid; K and L: Protein expression of GCLC, GSS, GCLM, and GPX4 in HGC-27 and MKN-45 cells transfected with the control or FXR-coding plasmid. ^aP < 0.05, ^bP < 0.01. These experiments were repeated three times. FXR: Farnesoid X receptor; GPX4: Glutathione peroxidase 4.