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. 2019 Mar 11;30(12):1521–1538. doi: 10.1089/ars.2017.7375

FIG. 1.

FIG. 1.

Increased renal damage and apoptosis were accompanied by enhanced renal expression of Cx32 protein in renal-IR-induced AKI. Male C57BL/6 mice that underwent renal IR were sacrificed at the time point of 6, 12, 24, and 48 h after reperfusion. Renal necrosis, renal tubular epithelial cells apoptosis, and Cx32 expression alternation were detected with different methods in kidneys. (A) Renal damage of mice at different reperfusion time points after renal IR (H&E; scale bar 50 μm). Blue arrow: tubular necrosis; red arrow: inflammatory cells; black arrow: cell swelling and cytoplasm rarefaction. (B–D) Kidney histopathology evaluation scores, levels of Cr and BUN at different reperfusion time points after renal IR. (E) Renal tubular epithelial cells apoptosis at different reperfusion time points after renal IR with TUNEL staining (scale bar 50 μm). (F) Renal Cx32 mRNA of mice at different reperfusion time points after renal IR with quantitative real-time polymerase chain reaction. (G, H) Renal Cx32 expression of mice at different reperfusion time points after renal IR with two different methods: Western blot analysis and IHC staining (scale bar 50 μm). Data are presented as mean ± SE (n = 8). *p < 0.05 versus sham group; #p < 0.05 versus 24 h after reperfusion group (F, G). AKI, acute kidney injury; BUN, blood urea nitrogen; Cr, creatinine; Cx32, connexin32; H&E, hematoxylin–eosin staining; IHC, immunohistochemistry; IR, ischemia reperfusion; TUNEL, terminal deoxynucleotidyl transferase dUTP nick-end labeling. Color images are available online.