Fig. 1.

CASP1-dependent pyroptosis plays a vital role in elevated IOP-induced retinal ischemic damage and RGCs loss. a HE staining and quantitative analysis of total retinal thickness in retina tissue harvested 7 days post RIR injury (n = 6). Scale bar: 50 μm. b Retrograde FG-labeled images and quantitative assay of RGCs survival in WT and GSDMD KO mice (n = 6). Scale bar: 200 μm. c Representative immunofluorescence images of RGCs in the retina. Anti-RBPMS was used to label RGCs (n = 6). Scale bar: 100 μm. d Western blot analysis of the indicated proteins (n = 6). The protein levels were normalized to β-actin levels. e Representative immunofluorescence images of RGCs in the retina from mice treated with or without CASP1 inhibitor. Anti-RBPMS was used to label RGCs (n = 6). Scale bar: 100 μm. f HE staining and quantitative analysis of total retinal thickness in retinal tissue (n = 6). Scale bar: 50 μm. g Retrograde FG-stained images and quantitative assay of RGCs amount from groups subjected to RIR and RIR concomitant with CASP1 suppression groups (200 μΜ, n = 6). Scale bar: 200 μm. WT: wide type; KO: knockout; RIR: retinal ischemia-reperfusion; GCL: ganglion cell layer; IPL: inner plexiform layer; INL: inner nuclear layer; OPL: outer plexiform layer; ONL: outer nuclear layer; CASP1 inh: caspase-1 inhibitor. All the experiments are representative of at least three independent experiments. Data are represented as the mean ± SD. *P < 0.05, **P < 0.01, one-way ANOVA and two-way ANOVA