Brain tissue saving effects by single-dose intralesional administration of Neuroprotectin D1 on experimental focal penetrating brain injury in rats.
Focal penetrating TBI
NPD1
Neuroprotectin D1
Traumatic brain injury
Journal
Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
ISSN: 1532-2653
Titre abrégé: J Clin Neurosci
Pays: Scotland
ID NLM: 9433352
Informations de publication
Date de publication:
Jun 2019
Jun 2019
Historique:
received:
04
12
2018
revised:
03
03
2019
accepted:
21
03
2019
pubmed:
6
4
2019
medline:
11
7
2019
entrez:
6
4
2019
Statut:
ppublish
Résumé
Traumatic brain injury (TBI) is followed by a secondary inflammation in the brain. Neuroprotectin D1 (NPD1) is synthesized from docosahexaenoic acid (DHA) and has anti-inflammatory and antiapoptotic effects in experimental models of neurodegenerative disease and brain ischemia-reperfusion. It is not known whether intralesional administration of NPD1 ameliorates inflammation and cell death after severe TBI. We therefore investigated the effects of NPD1 following a severe form of focal penetrating TBI. A total of 30 male Sprague-Dawley rats weighing between 350 and 450 g were exposed to focal penetrating TBI or sham surgery. The rats were randomized to NPD1 treatment (50 ng intralesionally, immediately following TBI) or no treatment. The rats were sacrificed at 24 or 72 h. All subgroups consisted of 5 rats. Brains were removed, fresh frozen, cut in 14-µm coronal sections and subjected to Fluoro-Jade, TUNEL, MnSOD, 3-NT, COX-2, Ox-42 and NF-κB immuno-staining and lesion size analyses. NPD1 decreased the lesion area at 72 h compared to no treatment with a mean change 42% (NPD1 14.1 mm
Identifiants
pubmed: 30948313
pii: S0967-5868(18)32093-9
doi: 10.1016/j.jocn.2019.03.032
pii:
doi:
Substances chimiques
Anti-Inflammatory Agents
0
protectin D1
0
Docosahexaenoic Acids
25167-62-8
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
227-233Informations de copyright
Copyright © 2019 Elsevier Ltd. All rights reserved.