Estimates of the quadratic models that established a relationship between inulin clearance and iohexol clearance for the CT and ARF groups.

<p>Estimates of the quadratic models that established a relationship between inulin clearance and iohexol clearance for the CT and ARF groups.</p

Estimates of Pearson’s linear correlation coefficients.

<p>CI, confidence interval.</p><p>^a Pearson’s linear correlation coefficient.</p><p>^b Interval of the 95% confidence for Pearson’s linear correlation coefficient</p><p>Estimates of Pearson’s linear correlation coefficients.</p

Distribution of inulin and iohexol clearances of all rats (CT and ARF).

<p>Distribution of inulin and iohexol clearances of all rats (CT and ARF).</p

Measurements of iohexol clearance, inulin clearance and creatinine (mg/dL) levels in control rats and in rats 1, 2, 3 and 4 days after cisplatin administration.

<p>Measurements of iohexol clearance, inulin clearance and creatinine (mg/dL) levels in control rats and in rats 1, 2, 3 and 4 days after cisplatin administration.</p

GSL-1 treatment induces transcripts for GM3 and GD3 synthases and the anti-apoptotic protein Bcl-2.

<p>BALB/c mice were injected at day 0 with 10 mg/kg of adriamycin (ADM) or treated concomitantly with ADM and 5 µg/mouse GSL-1 (ADM+GSL-1). (A) The ADM group showed decreased levels of ST8Sia1, the enzyme responsible for the generation of GD3 gangliosides, molecules that have been associated with podocyte physiology. In contrast, GSL-1 treatment increased the levels of this transcript compared with both control and ADM mice. (B) The levels of mRNA for GM3 synthase (ST3Gal5) were not altered in the ADM group; however, they were significantly augmented after GSL-1 treatment. Because GM3 gangliosides were associated with resistance to ADM-cytotoxicity due to Bcl-2 induction, we measured the mRNA levels of this protein in our system. (C) Bcl-2 transcripts were not altered by ADM but increased in ADM+GSL-1 mice, indicating a relationship between increased ST3Galt5 and Bcl-2 transcripts with renal protection from effects of ADM. * p<0.05 vs. control; # p<0.05 vs. ADM.</p

Pro and anti-inflammatory molecule expression in B1KO and wild type animals.

<p>All molecule expressions were measured by real-time PCR at 24 hours of reperfusion. B1KO group had lower pro-inflammatory molecule expression (T-bet and IL-1β) (A and B) and higher anti-inflammatory response (GATA-3, IL-4 and IL-10) (C, D and E). Statistical analyses were performed using the t-test.* B1KO <i>versus</i> B1B2WT, p<0.05.</p

Oligonucleotides sequence.

<p>Oligonucleotides sequence.</p

Cell death modulation under B1R-knockout.

<p>Apoptosis was estimated by Bcl-2 and Bad expression and caspase-3 activity, at 24 hours of reperfusion. Bcl-2 and Bad expression were measured by real-time PCR, and caspase-3 activity by fluorimetric assay. B1KO animals presented higher Bcl-2 expression (A) along with lower Bad expression (B) and caspase-3 activity (C), indicating a lower degree of apoptosis. Statistical analyses were performed using ANOVA.* B1KO <i>versus</i> B1B2WT and B2KO, p<0.05.</p

GSL-1 treatment inhibits ADM-induced renal failure due to podocyte injury in an iNKT-dependent manner.

<p>BALB/c WT or iNKT-deficient (Jalpha18^−/−) mice were injected at day 0 with 10 mg/kg of adriamycin (ADM) or treated concomitantly with ADM and 5 µg/mouse GSL-1 (ADM+GSL-1). (A) As a result of ADM cytotoxicity, the mice lost body weight in a time-dependent fashion, in contrast to the control, untreated mice, and the GSL-1-treated group. (B) The increased proteinuria/creatininuria found in the ADM group at day 7 post-ADM injection reflects impaired renal function compared with the control and ADM+GSL-1 animals. These data indicate a renoprotective effect of GSL-1 treatment. (C) The albuminuria levels found in ADM animals reflect the podocyte injury due to ADM cytotoxicity. In contrast, the albuminuria/creatininuria ratio in the ADM+GSL-1 group was comparable to that in the control animals, indicating podocyte conservation. The GSL-1 treatment failed to protect Jalpha18^−/− mice from ADM-induced renal injury, showing that its renoprotective effect is iNKT-dependent (D and E). * p<0.05 vs. control; # p<0.05 vs. ADM.</p

Renal IRI and bradykinin receptors expression.

<p>Bradykinin receptors were analyzed by real-time PCR. In B1B2WT, receptors expressions were cross-modulated (A). In B2KO, B1R expression was increased at 4 and 24 hours (B). Statistical analyses were performed by ANOVA. *B1R <i>versus</i> B2R, p<0.05. # B2KO <i>versus</i> B1B2WT, p<0.05.</p