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

FIG. 3.

FIG. 3.

Cx32 regulated the generation and distribution of ROS, which mediated IR-induced AKI. Cx32−/− and Cx32+/+ C57BL/6 mice that underwent renal IR were sacrificed at the time point of 24 h after reperfusion. (A, B) Cx32 gene deletion resulted in significant decrease of renal IR-induced intercellular ROS production (ROS stained in red with DHE; cell nuclei stained in blue with DAPI). Values expressed as mean ± SE (n = 8). *p < 0.05 compared with Cx32+/+ Sham group; #p < 0.05 versus Cx32+/+ IR group. When mice were pretreated with DPI (inhibitor of NADPH oxidase, 100 mg/kg) or NAC (a ROS scavenger, 200 mg/kg) for 1 h before renal IR: (C, D) ROS production of renal tissues was decreased obviously (ROS stained in red with DHE; cell nuclei stained in blue with DAPI), (E) Kidney histopathology damage and renal tubular epithelial cells apoptosis were reduced obviously (H&E and TUNEL; scale bar 50 μm). (F–G) levels of Cr and BUN were all attenuated. Data are presented as mean ± SE (n = 8). *p < 0.05 compared with Sham group; #p < 0.05 versus IR group. DAPI, 6-diamino-2-phenylindole; DHE, dihydroethidium, DPI, diphenyleneiodonium chloride; NAC, N-acetyl cysteine; ROS, reactive oxygen species. Color images are available online.