Effects of CORM01 on lung, liver, and kidney pathology of SS mice exposed to hemolysate
. | SS mice treated with saline buffer . | SS mice exposed to hemolysate and treated with vehicle . | SS mice exposed to hemolysate and treated with CORM-401 . |
---|---|---|---|
Lung | (n = 6) | (n = 6) | (n = 4) |
Inflammatory cell infiltrates | 7.6 ± 0.4 | 84.1 ± 2.9∗ | 26.4 ± 3.0∗,† |
Thrombi | 0 | + (1/6) | 0 |
Kidney | (n = 6) | (n = 6) | (n = 4) |
Inflammatory cell infiltrates | 0 | 6.62 ± 0.51∗ | 1.2 ± 0.014∗ |
Thrombi | 0 | 0 | 0 |
Fibrosis | 0 | 0 | 0 |
Liver | (n = 6) | (n = 6) | (n = 4) |
Inflammatory cell infiltrates | 9.2 ± 1.4 | 96 ± 2.8∗ | 44.1 ± 3.7∗,† |
Thrombi | 0 | + (1/6) | 0 |
Score | 2-2-2-2-1-1 | 3-3-2-3-3-3 | 2-2-3-2 |
. | SS mice treated with saline buffer . | SS mice exposed to hemolysate and treated with vehicle . | SS mice exposed to hemolysate and treated with CORM-401 . |
---|---|---|---|
Lung | (n = 6) | (n = 6) | (n = 4) |
Inflammatory cell infiltrates | 7.6 ± 0.4 | 84.1 ± 2.9∗ | 26.4 ± 3.0∗,† |
Thrombi | 0 | + (1/6) | 0 |
Kidney | (n = 6) | (n = 6) | (n = 4) |
Inflammatory cell infiltrates | 0 | 6.62 ± 0.51∗ | 1.2 ± 0.014∗ |
Thrombi | 0 | 0 | 0 |
Fibrosis | 0 | 0 | 0 |
Liver | (n = 6) | (n = 6) | (n = 4) |
Inflammatory cell infiltrates | 9.2 ± 1.4 | 96 ± 2.8∗ | 44.1 ± 3.7∗,† |
Thrombi | 0 | + (1/6) | 0 |
Score | 2-2-2-2-1-1 | 3-3-2-3-3-3 | 2-2-3-2 |
Lungs: Score for inflammatory cell infiltrate. Quantification of inflammatory cell infiltrates was expressed as the mean of cells per field at magnification of ×250, as resulting by the analysis of at least 10 different fields on each hematoxylin and eosin–stained whole-lung section (see also Brau et al28 and Fayad-Kobeissi et al29). Data are expressed as mean ± standard error of the mean (SEM); ∗P < .05 compared with normoxia; †P < .05 compared with vehicle.
Kidney: Score for inflammatory cell infiltrate. Quantification of inflammatory cell infiltration in renal cortex of kidney was determined in hematoxylin and eosin–stained sections using a 0 to 4 scale based on the percentage of cell infiltrates occupied area in each filed; 0 (no sign of infiltration), 1 (1%-10% of the area with cell infiltration), 2 (11%-25%); 3 (26%-50%), and 4 (50%). The mean of 15 randomly selected fields were analyzed at magnification ×400 (see also Belcher et al22 and Mpinganzima et al38). Data are expressed as mean ± SEM; ∗P < .05 compared with normoxia; †P < .05 compared with vehicle.
Liver score: 0, no hepatocellular damage; 1, mild injury characterized by cytoplasmic vacuolization and focal nuclear pyknosis; 2, moderate injury with dilated sinusoids, cytosolic vacuolization, and blurring of intercellular borders; 3, moderate to severe injury with noncoagulative necrosis, abundant sinusoidal dilatation, red blood extravasation into hepatic chords, hypereosinophilia, and migration of neutrophils; 4, severe necrosis with loss of hepatic architecture, disintegration of hepatic chords, hemorrhage, and neutrophils infiltration.
Statistical analysis: the nonparametric pairwise Wilcoxon rank-sum test was used. Each group was balanced in sex (50% males, 50% female). We repeated the comparisons for males and females separately with equivalent results. Regarding the sex, our data did not show evidence of differences between males and females.