Comim, Clarissa M; Barichello, Tatiana; Grandgirard, Denis; Dal-Pizzol, Felipe; Quevedo, João; Leib, Stephen L. (2013). Caspase-3 mediates in part hippocampal apoptosis in sepsis. Molecular neurobiology, 47(1), pp. 394-398. Clifton, N.J.: Humana Press 10.1007/s12035-012-8354-x
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The brain is one of the first organs affected during sepsis development resulting in apoptosis for a short-term and cognitive impairment for a long-term. Despite its importance, the mechanisms of brain dysfunction during sepsis are not fully elucidated. Thus, we here, in an animal model of sepsis, evaluated apoptosis in the dentate gyrus cell layer of the hippocampus to document the involvement of caspase-3 in the pathogenesis of neuronal apoptosis. Wistar rats sham-operated or submitted to the cecal ligation and perforation (CLP) procedure were killed at 12, 24, 48 h, and 10 days after surgery for the determination of caspase-3 and apoptosis rate. In a separate cohort of animals, a caspase-3-specific inhibitor was administered and animals were killed at 12 h after sepsis. An increase in the number of apoptotic cells 12, 24, and 48 h by histopathological evaluations and an increase of caspase-3 apoptotic cells 12 and 24 h after sepsis induction were observed. The caspase-3 inhibitor decreases the number of apoptotic cells by histopathological evaluations but not by immunohistochemistry evaluations. Caspase-3 is involved in part in apoptosis in the dentate gyrus cell layer of the hippocampus in septic rats submitted by CLP.
Item Type: |
Journal Article (Original Article) |
|---|---|
Division/Institute: |
04 Faculty of Medicine > Service Sector > Institute for Infectious Diseases |
UniBE Contributor: |
Leib, Stephen |
Subjects: |
500 Science > 570 Life sciences; biology 600 Technology > 610 Medicine & health |
ISSN: |
0893-7648 |
Publisher: |
Humana Press |
Language: |
English |
Submitter: |
Factscience Import |
Date Deposited: |
04 Oct 2013 14:38 |
Last Modified: |
05 Dec 2022 14:11 |
Publisher DOI: |
10.1007/s12035-012-8354-x |
PubMed ID: |
23054679 |
Web of Science ID: |
000316120500030 |
BORIS DOI: |
10.7892/boris.15179 |
URI: |
https://boris.unibe.ch/id/eprint/15179 (FactScience: 222446) |
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