Figure 2
Figure 2. Role of thrombin in vascular inflammation in SCD. (A-E) aPTT (A) and plasma levels of TAT (B), sVCAM-1 (C), IL-6 (D), and MPO (E) in the lungs of BERKAA (n = 9-10) and BERKSS (n = 10-12) mice that received dabigatran (Dab) or control placebo (Con) for 10 days. Formalin-fixed lungs were stained for neutrophils, and neutrophils were counted in 10 high-power fields (HPF; original magnification ×400) for each mouse. (F) Average number of neutrophils in 10 HPFs (×400) of lungs. (G) Representative lung sections demonstrating neutrophil infiltration in four different groups of mice. Neutrophils stain as brown. Asterisks directly above the bars indicate statistically significant difference between BERKSS compared with BERKAA mice within the same treatment group (Dab or Con) (*P < .05, **P < .01, and ***P < .001).

Role of thrombin in vascular inflammation in SCD. (A-E) aPTT (A) and plasma levels of TAT (B), sVCAM-1 (C), IL-6 (D), and MPO (E) in the lungs of BERKAA (n = 9-10) and BERKSS (n = 10-12) mice that received dabigatran (Dab) or control placebo (Con) for 10 days. Formalin-fixed lungs were stained for neutrophils, and neutrophils were counted in 10 high-power fields (HPF; original magnification ×400) for each mouse. (F) Average number of neutrophils in 10 HPFs (×400) of lungs. (G) Representative lung sections demonstrating neutrophil infiltration in four different groups of mice. Neutrophils stain as brown. Asterisks directly above the bars indicate statistically significant difference between BERKSS compared with BERKAA mice within the same treatment group (Dab or Con) (*P < .05, **P < .01, and ***P < .001).

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