Abstract | BACKGROUND: METHODS: Using a cortical cryogenic lesion model in mice, we investigated the impact of genetic deficiency of factor XII and inhibition of activated factor XII with a single bolus injection of recombinant human albumin-fused Infestin-4 on the release of bradykinin, the brain lesion size, and contact- kinin system-dependent pathological events. We determined protein levels of bradykinin, intracellular adhesion molecule-1, CC-chemokine ligand 2, and interleukin-1β by enzyme-linked immunosorbent assays and mRNA levels of genes related to inflammation by quantitative real-time PCR. Brain lesion size was determined by tetrazolium chloride staining. Furthermore, protein levels of the tight junction protein occludin, integrity of the blood-brain barrier, and brain water content were assessed by Western blot analysis, extravasated Evans Blue dye, and the wet weight-dry weight method, respectively. Infiltration of neutrophils and microglia/activated macrophages into the injured brain lesions was quantified by immunohistological stainings. RESULTS: CONCLUSIONS:
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Authors | Sarah Hopp, Marc W Nolte, Christian Stetter, Christoph Kleinschnitz, Anna-Leena Sirén, Christiane Albert-Weissenberger |
Journal | Journal of neuroinflammation
(J Neuroinflammation)
Vol. 14
Issue 1
Pg. 39
(02 20 2017)
ISSN: 1742-2094 [Electronic] England |
PMID | 28219400
(Publication Type: Journal Article)
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Chemical References |
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Topics |
- Animals
- Bradykinin
(metabolism)
- Brain Edema
(metabolism, prevention & control)
- Brain Injuries
(metabolism, prevention & control)
- Brain Injuries, Traumatic
(metabolism, prevention & control)
- Factor XIIa
(antagonists & inhibitors, genetics, metabolism)
- Inflammation
(metabolism, prevention & control)
- Male
- Mice
- Mice, Inbred C57BL
- Mice, Knockout
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