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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Biomaterials. 2015 Dec 2;80:96–105. doi: 10.1016/j.biomaterials.2015.11.062

Fig. 2. Salmon thrombin prevents vascular disruption dependent on protein C.

Fig. 2

(A) Mechanical allodynia (quantified by the number of paw withdrawals) is significantly reduced (**p=0.0148) on day 1 after compression treated with salmon thrombin (15min+STh) compared to human thrombin (15min+HTh). Allodynia for 15min+HTh is significantly greater (*p=0.016) than sham and not different from vehicle-treatment with compression (15min+veh). (B) There is minimal IgG labeling after 15min+STh in the ipsilateral dorsal horn on day 1, and is significantly less than 15min+HTh (*p<0.0001) and 15min+veh (#p=0.0009). Both 15min+HTh and 15min+veh exhibit robust ipsilateral spinal IgG labeling that is significantly greater (**p<0.0065) than the labeling in the respective contralateral sides. (C) HUVEC-lined microchannels exhibit increased FITC-dextran flux into the surrounding collagen when treated with TNF-α with or without serum. Salmon thrombin (TNF-α+STh) significantly reduces (*p=0.0073) TNF-α-induced flux compared to human thrombin (TNF-α+HTh) only in the presence of serum. TNF-α+STh and TNF-α+HTh are not different in serum-free conditions. (D) STh produces APC significantly faster (*p=0.008) than HTh. All data are mean±SD.