Skip to main content
. Author manuscript; available in PMC: 2016 Sep 16.
Published in final edited form as: Nature. 2016 Mar 16;531(7595):528–532. doi: 10.1038/nature17184

Figure 4. PGC1α effectors, Nam as therapy, and PGC1α in human AKI.

Figure 4

a, Serum creatinine in iNephPGC1α mice 24h after IRI with vehicle vs. mepenzolate (MPN, 10mg/kg IP) treatment (n=6/group). b, Serum creatinine in iNephPGC1α mice 24h after IRI with vehicle vs. indomethacin (INDO, 10mg/kg IP) treatment (n=6/group). c, Serial serum creatinines in mice receiving a single dose of Nam (400 mg/kg IP) 18h after the onset of reperfusion, i.e., with established AKI. Analyzed by ANOVA (n=5/group). d, Serial serum creatinines after cisplatin (25mg/kg IP administered on day 0) with or without Nam (400mg/kg IP on day −1 and day 0). Analyzed with Bonferroni-corrected ANOVA (n=5/group). e, Relative renal Nam from d. f,g, Representative immunostaining (brown) for PGC1α from control human kidney and a renal biopsy for AKI. Scale bars 50μm. h, PGC1α immunostaining intensity (1=weakest, 4=strongest). Each dot represents a unique specimen. Analyzed by Mann-Whitney. Error bars SEM, *p<0.05, **p<0.01, ****p<0.0001.