Nuclear factor-κB and apoptosis in patients with intracerebral hemorrhage

Studies using rat models have indicated that neuronal apoptosis is involved in the pathogenesis of intracerebral hemorrhage (ICH): however, the mechanism by which apoptosis occurs is unclear. In the present study, we aimed to quantify the number of nuclear factor-kappa B (NF-kappa B)-positive cells and apoptotic cells in specimens of middle temporal gyrus taken from 46 human subjects with hypertensive ICH. We also investigated the roles that intercellular adhesion molecule-1 (ICAM-1) and interleukin (IL)-1 beta play in apoptosis following ICH. At about 24 hours after ICH, some neurons exhibited nuclear swelling and incomplete cellular structures were visible. The mean percentage of apoptotic cells was 39.28 +/- 21.83% at 49-72 hours after ICH. NF-kappa B immunoreactivity varied with time after ICH: the number of immunostained neurons increased during the 2-6 hours after ICH, and reached a maximum at 7-48 hours. The number of IL-1 beta-immunostained neurons reached a maximum at 2-6 hours after ICH. The number of ICAM-1-immunostained neurons increased during the 48 hours after ICH and reached a maximum at 49-72 hours. These observations indicate that apoptosis has a major role in pathological cell death after ICH and that activation of NF-kappa B is positively related to the progress of apoptosis. Additionally, activation of ICAM-1 and IL-1 beta seem to be involved in apoptosis after ICH. (C) 2011 Elsevier Ltd. All rights reserved.