Objective       To determine the protective effect of sulfiredoxin-1 (Srxn1) on the injured astrocytes induced by oxygen-glucose deprivation/reoxygenation (OGD/R).       Methods       Lentivirus vector encoding Srxn1-shRNAs and a negative control were used to transfect to primary rat cortical astrocytes. Real-time quantitative PCR (q-PCR) and Western blotting were used to detect the expression of Srxn1 at mRNA and protein levels. The OGD/R model of astrocytes was established by OGD for 6 h followed by reoxygenation for 12 h to construct an in vitro model of ischemia reperfusion (for transfected cells

the establishment was started in 72 h after transfection). Then the normal control astrocytes were cultured under or not OGD/R

so were the astrocytes transfected by sh-Srxn1 or negative shRNAs. After reoxygenation for 12 h

the expression of Srxn1 was measured by q-PCR and Western blotting. Cell viability was determined by MTS assay. Apoptosis was measured by Hoechst 33342 staining. And the levels of Bcl-2 and Bax were measured by Western blotting.       Results       After transfection of sh-Srxn1

the mRNA and protein expression levels of Srxn1 were significantly decreased by 47.0% and 58.5% than the cells without transfection and negative control group. MTS assay indicated that interference of Srxn1 resulted in a decrease of cell viability compared with control+OGD/R group (38.79±2.14 vs 69.35±10.54

P0.05). Hoechst 33342 staning displayed that the apoptotic rate was significantly higher in sh-Srxn1+OGD/R group than in control+OGD/R group (51.67±7.64 vs 25.00±5.00

P0.01). And Western blotting showed that Srxn1 interference resulted in a decrease in Bcl-2 expression (P0.05)

an increase in Bax expression (P0.05)

and a significant decrease in the ratio of Bcl-2/Bax (P0.01)

when compared with control+OGD/R group.       Conclusion       Srxn1 exerts a protective effect on the oxidative stress injury in the astrocytes induced by OGD/R

which might be due to its anti-apoptosis effect.