C1 Esterase Inhibitor Reduces BBB Leakage and Apoptosis in the Hypoxic Developing Mouse Brain.
Animals
Animals, Newborn
Apoptosis
/ drug effects
Blood-Brain Barrier
/ drug effects
Brain
/ drug effects
Complement C1 Inhibitor Protein
/ pharmacology
Disease Models, Animal
Dual Specificity Phosphatase 1
/ biosynthesis
Female
Gene Expression Regulation, Developmental
/ drug effects
Hypoxia
/ drug therapy
Hypoxia, Brain
/ drug therapy
Inflammation Mediators
/ metabolism
Membrane Proteins
/ biosynthesis
Mice
Mice, Inbred C57BL
Mitochondrial Proteins
/ biosynthesis
Nerve Tissue Proteins
/ biosynthesis
Occludin
/ biosynthesis
Pregnancy
RNA, Messenger
/ biosynthesis
Random Allocation
S100 Calcium Binding Protein beta Subunit
/ biosynthesis
Tight Junction Proteins
/ biosynthesis
BNIP3
DUSP1
Hypoxia
Matrix metalloproteinases
Neonatal brain injury
Neuroprotection
Occludin
S100b protein
Tight junctions
Journal
Neuromolecular medicine
ISSN: 1559-1174
Titre abrégé: Neuromolecular Med
Pays: United States
ID NLM: 101135365
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
11
03
2019
accepted:
31
07
2019
pubmed:
16
8
2019
medline:
24
7
2021
entrez:
16
8
2019
Statut:
ppublish
Résumé
Inflammatory pathways involved in blood-brain barrier (BBB) vulnerability and hypoxic brain oedema in models of perinatal brain injury seem to provide putative therapeutic targets. To investigate impacts of C1-esterase inhibitor (C1-INH; 7.5-30 IU/kg, i.p.) on functional BBB properties in the hypoxic developing mouse brain (P7; 8% O
Identifiants
pubmed: 31414384
doi: 10.1007/s12017-019-08560-8
pii: 10.1007/s12017-019-08560-8
doi:
Substances chimiques
BNip3 protein, mouse
0
Complement C1 Inhibitor Protein
0
Inflammation Mediators
0
Membrane Proteins
0
Mitochondrial Proteins
0
Nerve Tissue Proteins
0
Occludin
0
Ocln protein, mouse
0
RNA, Messenger
0
S100 Calcium Binding Protein beta Subunit
0
S100b protein, mouse
0
Tight Junction Proteins
0
Dual Specificity Phosphatase 1
EC 3.1.3.48
Dusp1 protein, mouse
EC 3.1.3.48
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
31-44Références
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