Transcription factor nuclear factor-kappa-B (NFκB) is an important nuclear transcription factor, which initiates transcription of genes associated with immune responses and inflammation [12, 13] and also plays a key role in regulating inflammation in brain pathologies. It has been reported that NFκB increased in the region of perihematoma after ICH [14]. NFκB activation occurs within minutes and persists for at least a week in response to ICH, which is associated with the expression of selected target genes [15]. Activation of NFκB initiates inflammatory responses and contributes to the pathobiology of perilesional cell death after ICH [16]. Inhibition of NFκB activity has been shown to have a therapeutic effect on experimental ICH, such as reduce inflammation, behavioral dysfunction, and neuronal damage produced by ICH [17]. The knowledge about how NFκB is activated in the brain subjected to ICH is critical for seeking a new neuroprotective method for ICH.