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. 2013 Aug 15;4(8):e771. doi: 10.1038/cddis.2013.299

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Copyright © 2013 Macmillan Publishers Limited

This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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JNK mediates denitrosylation and activation of procaspase-3 during I/R in hippocampus. (a) Procaspase-3 denitrosylation, (b) procaspase-3 activation, (c) level of FasL, (d) level of Trx2 were measured followed by 3 h reperfusion (a) or 6 h reperfusion (b–d). SP600125 (30 mM), an inhibitor of JNK, was administrated 20 min before ischemia. The samples were processed using the biotin switch method followed by western blotting. SP600125 inhibited the denitrosylation and activation of procaspase-3 and the upregulated expression of FasL and Trx-2 after I/R. n=4; *P<0.05 compare with sham group, ^#P<0.05 compare with DMSO (I/R) group. Data are represented as means±S.D.