Fig. 9From: TRPV4-induced Müller cell gliosis and TNF-α elevation-mediated retinal ganglion cell apoptosis in glaucomatous rats via JAK2/STAT3/NF-κB pathwayTRPV4 activation led to increased phosphorylation of JAK2 and STAT3, thereby inducing NF-κB p65 translocation from the cytoplasm into the nucleus. A, C Immunoblotting analysis showing that GSK101 treatment increased the phosphorylation of STAT3 and JAK2, compared with the control group, but had no effect on the protein levels of JAK2 and STAT3 (C). B, D Bar charts summarizing mean expression levels of phosphorylated STAT3/STAT (B) and phosphorylated JAK2/JAK2 (D) under different conditions. n = 3 for all groups, *p < 0.05 and **p < 0.01. E, G Immunoblotting analysis showing that GSK101 treatment had no effect on the protein levels of NLRP3 (E) and caspase-1 (G), compared with the control group. F, H Bar charts summarizing mean expression levels of NLRP3 (F) and caspase-1 (H) under different conditions. n = 3 for all groups. I Confocal laser microphotographs of cultured Müller cells, stained with an antibody against NF-κB p65 (green), showing changes in NF-κB p65 protein expression in saline treatment (control), GSK101 treatment (GSK101), and HC Plus GSK101 (HC + GSK101) groups (a1–a3). b1–b3 are DAPI images. c1–c3 are merged images. Scale bar, 10 μm (for all images). J Bar graph summarizing mean density of NF-κB p65 immunofluorescence in Müller cells under different conditions. n = 3 for all groups. *p < 0.05. K Immunoblotting analysis showing that GSK101 treatment enhanced the expression of NF-κB p65 in Müller cell nuclei, compared with the control and preapplication of HC groups. L Bar chart summarizing mean expression levels of NF-κB p65 under different conditions. n = 5, *p < 0.05 and **p < 0.01Back to article page