Suppression of JNK pathway protects neurons from oxidative injury via attenuating parthanatos in glutamate-treated HT22 neurons.
Oxidative Stress
/ drug effects
Neurons
/ metabolism
Animals
Glutamic Acid
/ metabolism
Mice
Reactive Oxygen Species
/ metabolism
Parthanatos
/ drug effects
MAP Kinase Signaling System
/ drug effects
Apoptosis Inducing Factor
/ metabolism
Poly (ADP-Ribose) Polymerase-1
/ metabolism
Cell Line
Cell Survival
/ drug effects
Mitochondria
/ metabolism
JNK Mitogen-Activated Protein Kinases
/ metabolism
Anthracenes
/ pharmacology
Apoptosis
/ drug effects
Cell death
JNK
Neurons
Parthanatos
ROS
Journal
Scientific reports
ISSN: 2045-2322
Titre abrégé: Sci Rep
Pays: England
ID NLM: 101563288
Informations de publication
Date de publication:
28 10 2024
28 10 2024
Historique:
received:
20
05
2024
accepted:
15
10
2024
medline:
29
10
2024
pubmed:
29
10
2024
entrez:
29
10
2024
Statut:
epublish
Résumé
Oxidative stress causes diverse neurological disorders. Parthanatos is a type of programmed cell death, characterised by strong activation of poly (ADP-ribose) (PAR) polymerase-1 (PARP-1), PAR polymer accumulation, and nuclear translocation of apoptosis-inducing factor (AIF), and is involved in cellular oxidative injury. Signalling by c-Jun-N-terminal protein kinase (JNK) is activated by reactive oxygen species (ROS), and this also contributes to ROS production. However, the exact relationship between JNK signalling and parthanatos in neurological disorders triggered by oxidative stress is unclear. In this study, glutamate-treated HT22 neurons were used to investigate whether the signalling by JNK contributes a regulatory role to parthanatos in oxidative stress-related neurological disease. JNK signalling was activated in glutamate-treated HT22 neurons, demonstrated via upregulation of p-JNK levels. Pre-treatment with SP600125 markedly inhibited JNK signalling, increased cell viability, and significantly reversed PARP-1 overproduction, PAR polymer accumulation, and nuclear AIF translocation. In addition, inhibition of JNK signalling severely reduced the production of both intracellular ROS and mitochondria superoxide. This study indicated that parthanatos in glutamate-treated HT22 neurons could be suppressed by JNK signalling inhibition. JNK activation participated in parthanatos via an increase in intracellular ROS levels.
Identifiants
pubmed: 39468165
doi: 10.1038/s41598-024-76640-2
pii: 10.1038/s41598-024-76640-2
doi:
Substances chimiques
Glutamic Acid
3KX376GY7L
Reactive Oxygen Species
0
Apoptosis Inducing Factor
0
Poly (ADP-Ribose) Polymerase-1
EC 2.4.2.30
pyrazolanthrone
1TW30Y2766
JNK Mitogen-Activated Protein Kinases
EC 2.7.11.24
Anthracenes
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
25793Informations de copyright
© 2024. The Author(s).
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