Fig. 5: TMEM16A regulates hepatic I/R injury in a GPX4-dependent manner.
A Lipid ROS levels of primary hepatocytes isolated from indicated mice treated with RSL3 (3 μmoL/L) for 8 h followed by 4 h of hypoxia and 12 h of reoxygenation (n = 6). Red, reduced form of C11-BODIPY; a green, oxidized form of C11-BODIPY. *P < 0.05, **P < 0.01 versus TMFlox DMSO; ##P < 0.01 versus TMLKO DMSO. B Levels of pro-inflammatory factors (TNF-α, MCP-1, and CXCL-1) and C LDH release in indicated hepatocytes treated with RSL3, Erastin (10 μmoL/L), or Ferrostatin-1 (Fer, 2 μmoL/L) for 8 h followed by 4 h of hypoxia and 12 h of reoxygenation (n = 6). *P < 0.05, **P < 0.01 versus TMFlox DMSO or AAV-Con DMSO; ##P < 0.01 versus TMLKO DMSO or AAV-TM DMSO. D Representative 4-HNE immunohistochemical staining of liver samples from TMLKO and TMFlox mice injected with AAV-GPX4 shRNA via tail vein two weeks prior to I/R surgery (n = 6). E Representative H&E staining of liver sections, necrotic area quantification (area outside the contour indicates the injured part in the last two pictures on the right side), and F serum ALT and G AST levels in indicated mice (n = 6). *P < 0.05, **P < 0.01 versus TMFlox AAV-Scr shRNA; ##P < 0.01 versus TMLKO AAV-Scr shRNA. H Expression of proteins associated with the NF-κB signaling pathway in liver samples from indicated mice (n = 6). c versus TMFlox AAV-Scr shRNA; ##P < 0.01 versus TMLKO AAV-Scr shRNA. Data were presented as the mean ± SD.
