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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: Endothelial CXCR2 deficiency attenuates renal inflammation and glycocalyx shedding through NF-κB signaling in diabetic kidney disease

Fig. 5

CXCR2 overexpression in GECs aggravates renal glycocalyx degradation and inflammation via the NF-κB p65 signaling pathway. A Immunofluorescence was used to detect the expression of heparan sulfate in GECs. B Mean intensity of heparan sulfate (× 200, Scale bar = 50 μm, n = 3). C ELISA was used to measure the level of heparan sulfate in the supernatant of four groups of cells. D Immunofluorescence was used to detect the expression of syndecan-1 in GECs. E Mean intensity of syndecan-1 (× 200, Scale bar = 50 μm, n = 3). F ELISA was used to measure the level of syndecan-1 in the supernatant. G and H The protein levels of p-IKKβ, IKKβ, p-IκBα, IκBα, p-NF-κB p65, and NF-κB p65 were detected by western blotting. β-Actin was used as an internal reference control. The immunofluorescence staining (I) and mean intensity of E-selectin (J) (× 200, Scale bar = 50 μm, n = 3). qPCR assay was used to test the level of E-selectin (K). Representative images were shown. Results are expressed as mean ± SEM; **P < 0.01 vs. control group; &&P < 0.01 vs. HG + pcDNA3.1 group; ##P < 0.01 vs. HG + pcDNA3.1-CXCR2group; * P < 0.05, ** P < 0.01 and *** P < 0.001 vs. control group; & P < 0.05, && P < 0.01, &&& P < 0.001 vs. HG group; # P < 0.05, ### P < 0.001 vs. HG + pcDNA3.1-CXCR2 group; HG:high glucose

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