Fig. 9

GSK872 and Nec-1 inhibited RIP1/RIP3/MLKL pathway activation induced by glutamate excitotoxicity. a Expression levels of RIP1, RIP3, MLKL and p-MLKL (phospho S345) in R28 cells after exposure to 10 mM glutamate for 24 h with or without the addition of GSK872 or Nec-1. b Intravitreal administration of GSK872 or Nec-1 downregulated protein levels of RIP1, RIP3 and p-MLKL (phospho S345) in NMDA-damaged eyes. c Representative immunofluorescence microphotographs of retinal sections stained with RBPMS (green), RIP1 (red), and DAPI (blue) at 5 days post GSK872 and Nec-1 injection. Scale bar = 50 μm. d Representative immunofluorescence microphotographs of retinal sections stained with RBPMS (green), RIP3 (red), and DAPI (blue) at 5 days post GSK872 and Nec-1 injection. Scale bar = 50 μm. GCL: ganglion cell layer; INL: inner nuclear layer; ONL: outer nuclear layer; CTL: the control group; Glu: glutamate. The results were recorded as mean ± SD from at least three independent experiments. **p < 0.01, ***p < 0.001, ****p < 0.0001 versus control or saline group; ^#p < 0.05, ^##p < 0.01, ^###p < 0.001 versus Glu + DMSO group or NMDA + DMSO group. ns: not significant