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Intracerebral hemorrhage-induced brain injury is aggravated in senescence-accelerated prone mice
- Intracerebral hemorrhage-induced brain injury is aggravated in senescence-accelerated prone mice
- Lee J.-C.; Cho G.-S.; Choi B.-O.; Hyoung C.K.; Kim Y.-S.; Kim W.-K.
- Ewha Authors
- 김원기; 최병옥
- Issue Date
- Journal Title
- vol. 37, no. 1, pp. 216 - 222
- SCI; SCIE; SCOPUS
- Background and Purpose - In cerebral stroke, the overall mortality rate of older individuals is higher than that of younger individuals. We therefore investigated aging-related changes in brain tissue damage and immune response in response to intracerebral hemorrhage (ICH) in mice. Methods - ICH was induced by microinjecting autologous whole blood (5 μL) into the striatum of 4- or 14-month-old senescence-accelerated prone (SAMP8) mice or senescence-accelerated resistant (SAMR1) mice. Results - In all groups, neurological deficits occurred within 6 hours and gradually improved after the first day, but improvement was most delayed in 14-month-old SAMP8 mice. Isolectin B4-positive and amoeboid microglia/macrophages were abundantly distributed around and inside the hemorrhagic lesions in 14-month-old SAMP8 mice. In contrast, myeloperoxidase-immunoreactive neutrophils and reactive astrocytes with intensified glial fibrillary acidic protein-stained processes and swollen cytoplasm did not differ in number or distribution between SAMP8 and SAMR1 mice. Regardless of their age, the immunoreactivity of Mn-SOD, a major antioxidant enzyme in mitochondria, was much weaker in SAMP8 than in SAMR1 mice. The expression of inducible nitric oxide, however, was higher in old SAMP8 mice than in the other experimental groups. Conclusions - These results suggest that activated microglia/monocytes may aggravate intracerebral hemorrhagic damage in old SAMP8 mice. Further studies on the exact role of activated microglia/monocytes and the altered activities of antioxidant enzymes in old SAMP8 mice may provide useful information for ICH-induced brain injury in relation with aging. © 2005 American Heart Association, Inc.
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