Abstract
Thioredoxin-1 (Trx1) has long been recognized as a redox regulator, and is implicated in the inhibition of cell apoptosis. Trx1 is essential for the maintenance of the S-nitrosylation of molecules in cells. The S-nitrosylation of Trx1 is essential for the physiological function such as preservation of the redox regulatory activity. The mechanisms underlying Trx1 denitrosylation induced by kainate acid (KA) injection still remain uncharacterized. Our results showed that the S-nitrosylation levels of Trx1 were decreased subsequent to KA injection and that the glutamate receptor 6 (GluR6) antagonist NS102 could inhibit the denitrosylation of Trx1. Moreover, the denitrosylation of Trx1 following KA treatment could be suppressed by the Fas ligand (FasL) antisense oligodeoxynucleotides (AS-ODNs), the Trx reductase (TrxR) inhibitor dinitrochlorobenzene (DNCB), or the Nitric oxide (NO) donors sodium nitroprusside (SNP) and S-nitrosoglutathione (GSNO). Subsequently, these mechanisms were morphologically validated by cresyl violet staining, in situ TUNEL staining to detect the survival of CA1 and CA3/DG pyramidal neurons. NS102, FasL AS-ODNs, GSNO and SNP could provide neuroprotection of the pyramidal neurons of CA1 and CA3/dentate gyrus (DG) regions by attenuating Trx1 denitrosylation. Our results also showed that the denitrosylation of Trx1 induced by KA injection can active the caspase-3 which results in apoptosis.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
