Effects of aging on complement activation and neutrophil infiltration after intracerebral hemorrhage.

Intracerebral hemorrhage (ICH)-induced brain edema and neurological deficits are greater in aged rats than in young rats. Complement activation and neutrophil infiltration contribute to brain injury after ICH. In this study, we investigated the effects of aging on activation of the complement cascade and neutrophil influx following ICH. Male Sprague-Dawley rats (3 or 18 months old) received an infusion of 100 microL autologous blood into right caudate. Rats were killed at 1, 3, 7, and 28 days after ICH and the brains were sampled for immunohistochemistry and Western blot analysis. Levels of complement factor C9 and clusterin were used as markers for complement activation, and myeloperoxidase (MPO) staining was performed to detect neutrophil infiltration. Western blot analysis showed that complement C9 and clusterin levels in ipsilateral basal ganglia after ICH were higher in aged rats than in young rats (p < 0.05). Immunohistochemistry showed there were more C9- and clusterin-positive cells around the hematoma in aged rats. However, MPO-positive cells in ipsilateral basal ganglia were fewer in aged rats (p < 0.05) after ICH. Our results suggest that ICH causes more severe complement activation and less neutrophil infiltration in aged rats. Clarification of the mechanisms of brain injury after ICH in the aging brain should help develop new therapeutic strategies for ICH.