Objective      To investigate the cerebral cortex inflammation of SD rats model of focal ce

rebral ischemia/reperfusion and the underlying mechanism of IKK-NBD peptides’ anti-inflammation effect.       Methods      The MCAO/R SD rats were randomly assigned to 3 groups

that is

sham operation group

model group and IKK-NBD group

and each group was further randomly divided into 2 subgroups with reperfusion of 1 and 7 d after 2 hours’ ischemia. IKK-NBD of 4 μL was injected into the right lateral ventricle in 2 h before model infliction. Neurobehavior was evaluated by Zea-Longa score. HE staining was used for pathological observation

Western blotting and quantitative RT-PCR for mRNA and protein expression levels of c-rel and IκappaBα (IκBα)

and ELISA for the contents of IL-1β and IL-10 in the ischemic cortex.       Results      IKK-NBD improved the behavioral recovery and reduced edema and necrosis after 1 and 7 d of reperfusion. The protein expression of c-rel in the cell nucleus was significantly higher in the model group than in the sham operation group (

P

0.05)

but significantly lower in IKK-NBD group than model group in 1 and 7 d after reperfusion (

P

0.05

P

0.01)

while

in 1 d after reperfusion

it was significantly higher in IKK-NBD group than the sham operation group (

P

0.05). It was continuously decreased in the IKK-NBD group and model group with the elapse of time (

P

0.05). Expression level of IκBα mRNA was significantly higher in the model and IKK-NBD groups than the sham operation group in 1 and 7 d after reperfusion (

P

0.05)

with that in day 7 lower than in day 1

and it was higher in IKK-NBD group than in model group in 1 d after reperfusion (

P

0.01). IL-1β and IL-10 were significantly higher in the model and IKK-NBD groups than the sham operation group in 1 and 7 d after reperfusion (

P

0.01)

and continued to reduce with the time

but in the day 1

IL-1β was lower in the IKK-NBD group than in the model group (

P

0.01)

and IL-10 was higher in the IKK-NBD group than in the model group for the days 1 and 7 (

P

0.01).       Conclus

ion      IKK-NBD prevents c-rel against nuclear translocation by up-regulating IκBα in early stage after focal cerebral I/R

and thereby attenuates the inflammatory damages by down-regulating IL-1β and up-regulating IL-10. However

in later period after focal cerebral I/R

mild expression of c-rel exerts its anti-inflammatory effect by up-regulating IL-10.