Fig 1: DNA-PKcs deletion reduces LPS-mediated mitochondrial oxidative stress and apoptosis in hepatocytes. (A-C) Immunofluorescence staining of mitochondrial ROS and cytoplasmic ROS was performed in control and DNA-PKcs-depleted L02 hepatocytes following LPS treatment. (D-F) ELISA was used to analyze changes in SOD, GPX, and GSH expression in cultured liver cells. (G-H) The expression of caspase-3 and caspase-9 was measured in LPS-exposed hepatocytes through ELISA. (I-J) ELISA analysis of Bax expression and mPTP opening. *p < 0.05.
Fig 2: ROS and oxidative stress markers. (A) Perls Prussian Blue staining for ferric iron: representative 40× images (left) and quantification (right chart). DFO treatment decreased mean free iron in the dermis compared with IR Control and Normal Skin (*p < 0.05, **p < 0.01, ****p < 0.0001). (B) Representative 20× 8-Iso images (left) and quantification (right chart). DFO treatments decreased ROS-mediated lipid peroxidation compared with IR Control skin (****p < 0.0001). (C) ELISA of glutathione oxidation state (left chart) and BAX protein levels (right chart). DFO treatment decreased ratio of GSSG:GSH compared with IR Control skin (****p < 0.0001). DFO treatment also decreased BAX apoptotic protein level compared with IR Control skin (****p < 0.0001). Greater reduction in GSSG:GSH and BAX protein for DFO Patch relative to Injection were noted. Abbreviations: 8-Iso, 8-Isoprostane; BAX, Bcl-2-associated protein X; DFO, deferoxamine; ELISA, enzyme-linked immunosorbent assay; GSSG:GSH, ratio of oxidized to reduced glutathione; Inj, injection; ns, not significant; ROS, reactive oxygen species
Supplier Page from Abcam for Mouse Bax ELISA Kit