Apilarnil: A Novel Neuroprotective Candidate.
Blood-brain barrier; Brain; Sepsis; Apoptosis; Oxidative stress; Neurodegeneration.
Journal
Acta neurologica Taiwanica
ISSN: 1028-768X
Titre abrégé: Acta Neurol Taiwan
Pays: China (Republic : 1949- )
ID NLM: 9815355
Informations de publication
Date de publication:
30 Jun 2020
30 Jun 2020
Historique:
entrez:
22
5
2020
pubmed:
22
5
2020
medline:
1
8
2020
Statut:
ppublish
Résumé
This study was designed to investigate the effect of apilarnil on neuronal damage and related mechanisms in a sepsis model in order to demonstrate whether or not apilarnil has neuroprotective effect. In this study, 64 adult male Sprague-Dawley species rats were randomly divided into eight groups. The rats were administered apilarnil and/or lipopolysaccharide (LPS). Superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), xanthine oxidase (XOD) and testican-1 levels were measured in the brain tissue. Proinflammatory cytokines (tumor necrosis factor alpha [TNF-α], interleukin 1 beta [IL-1β], interleukin 6 [IL-6]) were measured in brain tissue. Histological examinations were performed on hippocampus and cortex tissues in all groups. Apoptotic cell count was estimated using the Tunel method to observe the apilarnil's effect on apoptosis. Purkinje cells were counted in the hippocampus to measure the protective effect of apilarnil on the hippocampus. Apilarnil reduced the decrease in SOD and CAT levels in the brain developing sepsis. Apilarnil reduced the increase in MDA, XOD, and testican-1 levels in the septic brain. It was observed that the number of degenerated neurons due to sepsis decreased as apilarnil dose increased. Apilarnil reduced the elevated levels of proinflammatory cytokines (IL-6, TNF-α, IL-1β) induced by sepsis. Apilarnil prevented sepsis-related apoptosis in the brain. The neuroprotective potential of apilarnil against brain damage in the sepsis model was demonstrated and suggested that it has the potential to contribute to new therapeutic targets against various neurological disorders.
Substances chimiques
Biological Products
0
Cytokines
0
Tumor Necrosis Factor-alpha
0
apilarnil
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM