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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: Deletion of angiotensin-converting enzyme 2 exacerbates renal inflammation and injury in apolipoprotein E-deficient mice through modulation of the nephrin and TNF-alpha-TNFRSF1A signaling

Fig. 5

ACE2 deficiency resulted in increases in oxidative stress levels in the ApoE/ACE2 DKO kidneys. a, b The real-time PCR analysis revealed mRNA expression of the NADPH oxidase subunits NOX2 (a) and NOX4 (b) in mice kidneys (n = 6). GAPDH was used as an endogenous control. c, d Representative dihydroethidium fluorescence images (c), relative fluorescence values and lucigenin-enhanced chemiluminescence assay (d) exhibited the superoxide generation and NADPH oxidase activity in mice kidneys. n = 5. WTC wild-type control, ApoE apolipoprotein E, ACE2 angiotensin-converting enzyme 2, KO knockout, DKO the ApoE/ACE2 double knockout. *P < 0.05; **P < 0.01 compared with WT control group; # P < 0.05 compared with ApoEKO group.

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