Figure 3.
ANV-6L15 blocked the TBI-induced hypercoagulable state. (A) TBI significantly shortened tail bleeding, measured 1 hour post-FPI, and this was partially reversed by ANV-6L15 (n = 7 mice per group, 1-way ANOVA). (B-E) The TBI-induced hypercoagulation and its blockage by ANV-6L15, as measured by thrombin generation (B) (graph: thrombin generation plots, bar-graph insert: peak-thrombin generation, n = 9 mice per group), clotting time (C), plasma fibrinogen (D), and D-dimer (E). The data in panels C-E was analyzed using 1-way ANOVA (n = 9 mice per group). (F-G) Representative images of intravascular fibrin deposition detected using PTAH stains in cerebral (F) (arrowhead: microvascular bleeding, arrow: fibrin; scale bar, 20 µm) and pulmonary interstitial microvessels (G) (red arrow: fibrin deposition; scale bar, 50 µm) of TBI mice (×20 objective).

ANV-6L15 blocked the TBI-induced hypercoagulable state. (A) TBI significantly shortened tail bleeding, measured 1 hour post-FPI, and this was partially reversed by ANV-6L15 (n = 7 mice per group, 1-way ANOVA). (B-E) The TBI-induced hypercoagulation and its blockage by ANV-6L15, as measured by thrombin generation (B) (graph: thrombin generation plots, bar-graph insert: peak-thrombin generation, n = 9 mice per group), clotting time (C), plasma fibrinogen (D), and D-dimer (E). The data in panels C-E was analyzed using 1-way ANOVA (n = 9 mice per group). (F-G) Representative images of intravascular fibrin deposition detected using PTAH stains in cerebral (F) (arrowhead: microvascular bleeding, arrow: fibrin; scale bar, 20 µm) and pulmonary interstitial microvessels (G) (red arrow: fibrin deposition; scale bar, 50 µm) of TBI mice (×20 objective).

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