Figure 5

Recombinant ADAMTS 13 blocked tPA neurotoxicity by reducing exogenous tPA/NR2B interactions and the activation of NR2B.

(A) Representative immunoblots and quantitative determinations of the levels of NR1, NR2A and NR2B in mice treated with vehicle, tPA, tPA in combination with rADAMTS 13 and rADAMTS 13 24 hours after MCA occlusion. The gels have been run under the same experimental conditions. Values are mean ± SD (n = 5 per group). *P < 0.05. (B) Interaction between tPA and NR2B detected by immunoprecipitation analysis in ischemic brain of mice treated with vehicle, tPA, rADAMTS 13 in combination with tPA and rADAMTS 13 24 hours after MCA occlusion. IP, immunoprecipitation; WB, Western blotting. Input, protein of the extracts without IP. The gels have been run under the same experimental conditions. Data are representative of three independent experiments. (C) Representative photographs of TTC stained coronal section and quantitative analysis of infarct volume in wild-type, ADMTS13^−/− mice and ADMTS13^−/− mice treated with tPA. Values are mean ± SD (n = 8 per group). *P < 0.05. (D) Representative photographs of TTC stained coronal section and quantitative analysis of infarct volume in mice treated with vehicle, tPA, tPA + rADAMTS 13, tPA + ifenprodil and tPA + rADAMTS 13 + ifenprodil 48 hours after MCA occlusion. Values are mean ± SD (n = 8 per group). *P < 0.05.