AEBP1 Silencing Protects Against Cerebral Ischemia/Reperfusion Injury by Regulating Neuron Ferroptosis and Microglia M2 Polarization Through PRKCA‐PI3K‐Akt Axis DOI
Yafen Zhang, Yan Li,

Fengli Liu

et al.

Drug Development Research, Journal Year: 2024, Volume and Issue: 85(8)

Published: Dec. 1, 2024

ABSTRACT Cerebral ischemia/reperfusion injury is one of the main causes neuronal damage. Neuron ferroptosis and microglia polarization are considered as critical processes during cerebral ischemia/reperfusion. Adipocyte enhancer‐binding protein 1 (AEBP1) usually acts a transcriptional repressor which involved in various diseases. However, it still remains unknown whether AEBP1 could have important roles regulating neuron injury. The oxygen‐glucose deprivation reperfusion (OGD/R)‐treated cells middle artery occlusion (MCAO)‐treated mice were used vitro vivo models. differentially expressed factors analyzed according to GEO datasets. Relative mRNA expression levels detected by qRT‐PCR western blot analysis. Cell viability was measured CCK‐8 assay. ROS, GSH iron contents using specifical assay kits. CD26 CD206 immunofluorescence Inflammatory cytokines ELISA. association between PRKCA assessed luciferase reporter ChIP analyses. damage TTC staining neurological deficit score. Transcription factor increased OGD/R‐treated HT22 BV2 cells. silencing attenuated OGD/R‐induced cell through increasing viability, GPX4 levels, decreasing ACSL4 levels. knockdown promoted M2 CD206‐positive Arg‐1 level, reducing iNOS, TNF‐α, IL‐1β IL‐6 transcriptionally repressed expression, further regulated PI3K/Akt signaling activation. Inhibition or reversed effects on polarization. downregulation infarct size scores MCAO‐treated mice. mitigated activating signaling, indicating potentially protective action

Language: Английский

NADPH Oxidases in Neurodegenerative Disorders: Mechanisms and Therapeutic Opportunities DOI
Mariana Bernardo Fiadeiro, João C. F. Diogo, Ana Silva

et al.

Antioxidants and Redox Signaling, Journal Year: 2024, Volume and Issue: 41(7-9), P. 522 - 541

Published: May 18, 2024

The nicotinamide adenine dinucleotide phosphate oxidase (NOX) enzyme family, located in the central nervous system, is recognized as a source of reactive oxygen species (ROS) brain. Despite its importance cellular processes, excessive ROS generation leads to cell death and involved pathogenesis neurodegenerative disorders.

Language: Английский

Citations

5
Buyang Huanwu decoction promotes gray and white matter remyelination by inhibiting Notch signaling activation in the astrocyte and microglia after ischemic stroke DOI
Man-zhong Li,

Yuming Zhuang,

Mingcong Li

et al.

Journal of Ethnopharmacology, Journal Year: 2025, Volume and Issue: unknown, P. 119440 - 119440

Published: Feb. 1, 2025

Language: Английский

Citations

0
AEBP1 Silencing Protects Against Cerebral Ischemia/Reperfusion Injury by Regulating Neuron Ferroptosis and Microglia M2 Polarization Through PRKCA‐PI3K‐Akt Axis DOI
Yafen Zhang, Yan Li,

Fengli Liu

et al.

Drug Development Research, Journal Year: 2024, Volume and Issue: 85(8)

Published: Dec. 1, 2024

ABSTRACT Cerebral ischemia/reperfusion injury is one of the main causes neuronal damage. Neuron ferroptosis and microglia polarization are considered as critical processes during cerebral ischemia/reperfusion. Adipocyte enhancer‐binding protein 1 (AEBP1) usually acts a transcriptional repressor which involved in various diseases. However, it still remains unknown whether AEBP1 could have important roles regulating neuron injury. The oxygen‐glucose deprivation reperfusion (OGD/R)‐treated cells middle artery occlusion (MCAO)‐treated mice were used vitro vivo models. differentially expressed factors analyzed according to GEO datasets. Relative mRNA expression levels detected by qRT‐PCR western blot analysis. Cell viability was measured CCK‐8 assay. ROS, GSH iron contents using specifical assay kits. CD26 CD206 immunofluorescence Inflammatory cytokines ELISA. association between PRKCA assessed luciferase reporter ChIP analyses. damage TTC staining neurological deficit score. Transcription factor increased OGD/R‐treated HT22 BV2 cells. silencing attenuated OGD/R‐induced cell through increasing viability, GPX4 levels, decreasing ACSL4 levels. knockdown promoted M2 CD206‐positive Arg‐1 level, reducing iNOS, TNF‐α, IL‐1β IL‐6 transcriptionally repressed expression, further regulated PI3K/Akt signaling activation. Inhibition or reversed effects on polarization. downregulation infarct size scores MCAO‐treated mice. mitigated activating signaling, indicating potentially protective action

Language: Английский

Citations

0