Abstract：
:Oxidative stress results in protein oxidation and is implicated in cerebral disease, such as Parkinson's disease, Alzheimer's disease, and ischemic stroke. Sulfiredoxin-1 (Srxn1) is an endogenous antioxidant protein that has neuroprotective effects. The mechanisms of Srxn1 in oxidative stress have not been well studied, however. This study used 180 μM H2 O2 exposure for 24 hr to model oxidative stress. This experimental design allowed us to explore the protective effects and underlying mechanisms of Srxn1 in PC12 cells. To investigate Srxn1's role in oxidative stress protection, transient knockdowns of Srxn1 in PC12 cells were performed prior to treatment with 180 μM H2 O2 for 24 hr. Knockdown of Srxn1 resulted in decreased cell viability and increased cellular damage as determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and lactate dehyrogenase analysis, respectively. Intracellular superoxide dismutase and glutathione are important indexes of oxidative stress; these were reduced in Srxn1 knockdown PC12. We further found that the decreased Srxn1 correlated with a reduction in 2-Cys Prdxs activity. Moreover, 2-Cys Prdxs protein levels were increased in the H2 O2 -dosed cells, as measured by RT-PCR and immunoblot analysis. These results suggested that Srxn1 can protect PC12 cells from H2 O2 -induced oxidative stress and are involve in Prdxs activity. Srxn1 play a protective role against oxidative injury and demonstrates potential as a target for neuroprotective intervention in oxidative stress.
journal_name
J Neurosci Resjournal_title
Journal of neuroscience researchauthors
Li Q,Yu S,Wu J,Zou Y,Zhao Ydoi
10.1002/jnr.23218subject
Has Abstractpub_date
2013-06-01 00:00:00pages
861-70issue
6eissn
0360-4012issn
1097-4547journal_volume
91pub_type
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