Deletion of Rac1GTPase in the Myeloid Lineage Protects against Inflammation-Mediated Kidney Injury in Mice
Fig 2
Lipopolysaccharide (LPS)-evoked renal functional and histological changes in M-Rac1 FC and KO mice.
Vehicle or LPS (5 mg/kg) was injected intraperitoneally in M-Rac1 FC and KO mice, and animals were sacrificed 48 h later. (A and B) Blood urea nitrogen (BUN) and serum creatinine. Data are expressed as means ± s.e.m. Statistical analysis was performed by two-way ANOVA, P < 0.01 genotype effect, P < 0.01 treatment effect, P < 0.01 interaction effect. **P < 0.01 by Bonferroni's post hoc test. n = 8 per each group. (C) The mRNA expression of kidney injury biomarkers, Kim-1 and Ngal, in the kidney homogenates of Vehicle- or LPS-injected M-Rac1 FC and KO mice. The mRNA levels were compared using real-time quantitative RT-PCR and expressed relative to M-Rac1 FC Vehicle group. Statistical analysis was performed by two-way ANOVA, P < 0.01 genotype effect, P < 0.01 treatment effect, P < 0.01 interaction effect. **P < 0.01 by Bonferroni's post hoc test. n = 8 per each group. (D) Typical images of hematoxylin-eosin stained kidney sections. Original magnification x 400. (E) Semiquantitative analysis of tubular injury. Data were analyzed using nonparametric analysis with Kruskal-Wallis test. **P < 0.01 by Mann-Whitney U test. n = 5 per each group.