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. Author manuscript; available in PMC: 2015 Jun 1.
Published in final edited form as: Kidney Int. 2014 Jun 11;86(6):1150–1160. doi: 10.1038/ki.2014.196

Figure 1.

Figure 1

SA-overload in rats induces proteinuria and glomerular expression of COX-2, pro-inflammatory and stress genes. A) Urinary protein/creatinine ratios (UP:CR) of the BSA-treated rats vs control rats (n=3 for each group; *P<0.05 versus control, determined by two way ANOVA Tukey's multiple comparisons test). B) Massive amounts of urinary albumin are excreted from BSA-treated rats but not control rats (representative gels are shown from each group). Urine was collected on five consecutive days and equal volumes (4 μl) analyzed by SDS-PAGE and Coomassie Brilliant Blue staining. C) Urinary albumin/creatinine ratio (UA:CR) of the BSA-treated rats vs control rats (n=3 for each group; *P<0.05 versus control, determined by two way ANOVA Tukey's multiple comparisons test). D) Total RNA was extracted from the isolated glomeruli of control and BSA-treated rats and relative mRNA levels of COX-2, pro-inflammatory and stress genes were measured by qRT-PCR and normalized to β-actin (*P<0.05, **P<0.01 and ***P<0.001 versus control, determined by t test).