Objective       To determine the protective effect of sulfiredoxin-1 (Srxn1) on cultured rat astrocytes after ischemic-induced injury and investigate whether the molecule takes part in the activation of NF-κB signaling pathway.       Methods       Hydrogen peroxide (H

2

O

2

) and oxygen-glucose deprivation followed by recovery (OGD/R) were respectively used to mimic cerebral ischemia damage stress in freshly isolated astrocytes from newborn SD rats. Lentiviral vectors c

arrying 2 shRNAs for Srxn1

Lenti-Srxn1-sh1 and Lenti-Srxn1-sh2

were used to knockdown Srxn1 in the astrocytes under the 2 models of ischemia. Cell viability was tested by MTT assay. The nuclear translocation of NF-κB was detected by double fluorescent immunoassay. The protein expression of p-NFκB p65 and macrophage migration inhibitory factor (MIF) was determined by Western blotting.       Results       Both lentiviral vectors induced decreased protein level of Srxn1 in the rat astrocytes after either H

2

O

2

or OGD/R treatment. Knockdown of Srxn1 resulted in obviously decreased cell viability

enhanced nuclear translocation of NF-κB p65

and up-regulated expression of p-NFκB p65 and MIF

when compared with the astrocytes without Srxn1 knowdown.       Conclusion       Srxn1

as an important neuroprotective factor

protects astrocytes from ischemia-induced injury

which might be due to its involving in the activation of NF-κB pathways.