Objective    To observe the expression of NF-κB and explore the effect of polydatin (PD) during ischemia-reperfusion (I-R) induced cortical neuron injury in vitro.     Methods    The cortical neurons from newborn SD rats cultured for 7 d were randomly divided into control group

model group and PD group. The morphological features of neuronal apoptosis were observed with AO/EB and DAPI staining. Apoptosis

Bcl-2/Bax

and the expressions of NF-κB p65 were determined 0

6

12

24

48 h after reperfusion.     Results    Typical morphological changes of neuronal apoptosis were observed in model group. The number of apoptotic cells and the expressions of NF-κB p65 increased with time prolongation after reperfusion (P0.05)

peaked 24 h after reperfusion

then decreased in model group compared with those in control group

while Bcl-2/Bax ratio peaked 6 h after reperfusion

then decreased (P0.05). The number of apoptotic cells and the expressions of NF-κB p65 were decreased in PD group compared with those in model group with statistical significance (P0.05)

while Bcl-2/Bax ratio was increased (P0.05).     Conclusion    The activation of NF-κB p65 participates in cerebral I-R injury. PD protects against in vitro I-R injury by decreasing neuron apoptosis that may be through suppressing NF-κB p65 activation and upregulating Bcl-2/Bax ratio.