Bimodal Distribution of Nuclear Factor-κB Activation and Expression of Subunits in Experimental Models of Intracerebral Hemorrhage In Vivo

Abstract Objective : The exact role of nuclear factor-kappaB (NF-κB) in intracerebral hemorrhage (ICH) is still unclear to date. The aim of the present study is to clarify the activation of NF-κB and the role of its subunits in inflammatory response and cell death after ICH. Methods : The model of ICH rats was made, and at preset time points after operation, as well as rats in the control and sham groups, the ipsilateral striatum and tissue around was obtained for detection of NF-κB activation, cell death, and expression of interleukin-1β, tumor necrosis factor-α, Caspase-3, Bcl-2, and NF-κB subunits. Results : There were 2 peaks of NF-κB activation (2 days and 10 days) after ICH. The expression of p50 and p65 reached the peak at 1 day and 2 day, leading to the first peak of NF-κB activation, and that of c-Rel at 10 day, leading to the second. The peak of cell death and caspase-3 expression, and the nadir of bcl-2 expression appeared to be synchronizing with or right after the first peak of NF-κB activation. Then, at the second peak of NF-κB activation, cell death, and caspase-3 expression decreased and the bcl-2 expression returned to the normal level. Conclusions : NF-κB activation showed a bimodal distribution mode after ICH. We can speculate that p50 and p65 may promote the inflammatory response and apoptosis, and c-Rel may play the opposite role. Measures might be performed at the different phases to reduce the brain injury in the early stage and promote the brain recovery in the late stage after ICH.