Effect of Apigenin on the Expression of NF-κB and iNOS in Transient Focal Cerebral Ischemia and Reperfusion Model of Rats

Objective:To study the neuroprotective effect of apigenin on transient focal cerebral ischemia and reperfusion injury in rats,which was characterized by its influence on nuclear factor-κappaB (NF-κB) and inducible nitric oxide synthase (iNOS) expression. Methods:One hundred and thirty five male Spragur-Dawley rats were randomized into 9 groups :sham-operated group(S,n=15); model groups(group M24h,group M48h,group M72h,group M7d,n=15)and apigenin-treated groups(group A24h,group A48h,group A72h,grouop A7d,n=15).The transient focal cerebral ischemia and reperfusion(1.5hours) model in rat was established with insertion of thread embolish into middle cerebral artery. The cellular and subcellular morphology under optic microscope and electromicroscope, the expression of NF-κB p65 by immuno-histochemistry (ICH ) and the activity of inducible nitric oxide synthase (iNOS) by colorimetric method were measured.Results:The expression of NF-κB p65 were significantly higher in group M (P0.01) , the positive expressions of NF-κB p65 in group A72h and A7d were obviously lower than ones in group M(P0.05).The activities of iNOS were significantly higher in group M than ones in group S respectively(P0.01), the activities of iNOS in group A72h and group A7d were significantly lower than ones at the corresponding time points in group M respectively(P0.05). Group M showed obvious intracellular and intercellular edema and vacuolization in ischemic cortexes and hippocampuses, especially in group M48h.There were karyopycnosis and organelle broaden and dissolution and vacuolization in glias and neurons, especially in group M24h. The cellular edema in group A was lessened compared to one in group M, cellular morphologic change was scarcely observed between group A and group M. Conclusion:Apigenin may play a neuroprotective effect which was related with depression of NF-κB activation and of the iNOS generation in transient focal cerebral ischemia and reperfusion of rats.