Systemic LPS administration induces brain inflammation but not dopaminergic neuronal death in the substantia nigra
It has been suggested that brain inflammation is important in aggravation of brain damage and/or that inflammation causes neurodegenerative diseases including Parkinson's disease (PD). Recently, systemic inflammation has also emerged as a risk factor for PD. In the present study, we evaluated h...
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Published in | Experimental & molecular medicine Vol. 42; no. 12; pp. 823 - 832 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.12.2010
Springer Nature B.V Korean Society for Biochemistry and Molecular Biology 생화학분자생물학회 |
Subjects | |
Online Access | Get full text |
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Summary: | It has been suggested that brain inflammation is important in aggravation of brain damage and/or that inflammation causes neurodegenerative diseases including Parkinson's disease (PD). Recently, systemic inflammation has also emerged as a risk factor for PD. In the present study, we evaluated how systemic inflammation induced by intravenous (iv) lipopolysaccharides (LPS) injection affected brain inflammation and neuronal damage in the rat. Interestingly, almost all brain inflammatory responses, including morphological activation of microglia, neutrophil infiltration, and mRNA/protein expression of inflammatory mediators, appeared within 4-8 h, and subsided within 1-3 days, in the substantia nigra (SN), where dopaminergic neurons are located. More importantly, however, dopaminergic neuronal loss was not detectable for up to 8 d after iv LPS injection. Together, these results indicate that acute induction of systemic inflammation causes brain inflammation, but this is not sufficiently toxic to induce neuronal injury. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 G704-000088.2010.42.12.003 http://kmbase.medric.or.kr/Main.aspx?d=KMBASE&m=VIEW&i=0620920100420120823 |
ISSN: | 1226-3613 2092-6413 2092-6413 |
DOI: | 10.3858/emm.2010.42.12.085 |