Adenosine A
A3AR
Cognitive impairment
NLRP3
Neuroinflammation
Traumatic brain injury
Journal
Journal of neuroinflammation
ISSN: 1742-2094
Titre abrégé: J Neuroinflammation
Pays: England
ID NLM: 101222974
Informations de publication
Date de publication:
12 Nov 2020
12 Nov 2020
Historique:
received:
24
07
2020
accepted:
22
10
2020
entrez:
13
11
2020
pubmed:
14
11
2020
medline:
27
8
2021
Statut:
epublish
Résumé
Traumatic brain injury (TBI) is a common pathological condition that presently lacks a specific pharmacological treatment. Adenosine levels rise following TBI, which is thought to be neuroprotective against secondary brain injury. Evidence from stroke and inflammatory disease models suggests that adenosine signaling through the G protein-coupled A Using the selective A When measured 24 h after controlled cortical impact (CCI) TBI, male mice treated with intraperitoneal injections of MRS5980 (1 mg/kg) had reduced secondary tissue injury and brain infarction than vehicle-treated mice with TBI. These effects were associated with attenuated neuroinflammation marked by reduced activation of nuclear factor of kappa light polypeptide gene enhancer in B cells (NFκB) and MAPK (p38 and extracellular signal-regulated kinase (ERK)) pathways and downstream NOD-like receptor pyrin domain-containing 3 inflammasome activation. MRS5980 also attenuated TBI-induced CD4 Our results provide support for the beneficial effects of small molecule A
Sections du résumé
BACKGROUND
BACKGROUND
Traumatic brain injury (TBI) is a common pathological condition that presently lacks a specific pharmacological treatment. Adenosine levels rise following TBI, which is thought to be neuroprotective against secondary brain injury. Evidence from stroke and inflammatory disease models suggests that adenosine signaling through the G protein-coupled A
METHODS
METHODS
Using the selective A
RESULTS
RESULTS
When measured 24 h after controlled cortical impact (CCI) TBI, male mice treated with intraperitoneal injections of MRS5980 (1 mg/kg) had reduced secondary tissue injury and brain infarction than vehicle-treated mice with TBI. These effects were associated with attenuated neuroinflammation marked by reduced activation of nuclear factor of kappa light polypeptide gene enhancer in B cells (NFκB) and MAPK (p38 and extracellular signal-regulated kinase (ERK)) pathways and downstream NOD-like receptor pyrin domain-containing 3 inflammasome activation. MRS5980 also attenuated TBI-induced CD4
CONCLUSION
CONCLUSIONS
Our results provide support for the beneficial effects of small molecule A
Identifiants
pubmed: 33183330
doi: 10.1186/s12974-020-02009-7
pii: 10.1186/s12974-020-02009-7
pmc: PMC7659122
doi:
Substances chimiques
Adenosine A3 Receptor Agonists
0
Receptor, Adenosine A3
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
339Subventions
Organisme : NINDS NIH HHS
ID : R01 NS111120
Pays : United States
Organisme : NINDS NIH HHS
ID : 1R01NS111120-01A1
Pays : United States
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