p38γ modulates ferroptosis in brain injury caused by ethanol and cerebral ischemia/reperfusion by regulating the p53/SLC7A11 signaling pathway DOI Creative Commons
Xingyu Zhu, Zhihan Zhao, Yan Zhang

et al.

Cellular Signalling, Journal Year: 2025, Volume and Issue: unknown, P. 111728 - 111728

Published: March 1, 2025

Ischemic stroke, a neurological condition with complicated etiology that is accompanied by severe inflammation and oxidative stress, ethanol (EtOH) may aggravate ischemia/reperfusion (I/R)-induced brain damage. However, the effect of prolonged alcohol intake on acute injury remains ambiguous. As part mitogen-activated protein kinase (MAPK) family, p38γ involved in ferroptosis various diseases. This study explored how effects chronic EtOH consumption caused cerebral I/R. Brain damage was induced mice via administration liquid alcohol-containing diet for 8 weeks, middle artery occlusion reperfusion (MCAO/R), or combination both. We verified significantly exacerbated MCAO/R-induced damage, inflammation. Notably, levels were increased experimental mouse cell models. knockdown markedly attenuated tissue inflammatory infiltration + MCAO/R-treated mice. Mechanistic experiments revealed regulate through p53/SLC7A11 pathway. Overall, our results indicate crucial regulating EtOH- I/R-induced modulating

Language: Английский

p38γ modulates ferroptosis in brain injury caused by ethanol and cerebral ischemia/reperfusion by regulating the p53/SLC7A11 signaling pathway DOI Creative Commons
Xingyu Zhu, Zhihan Zhao, Yan Zhang

et al.

Cellular Signalling, Journal Year: 2025, Volume and Issue: unknown, P. 111728 - 111728

Published: March 1, 2025

Ischemic stroke, a neurological condition with complicated etiology that is accompanied by severe inflammation and oxidative stress, ethanol (EtOH) may aggravate ischemia/reperfusion (I/R)-induced brain damage. However, the effect of prolonged alcohol intake on acute injury remains ambiguous. As part mitogen-activated protein kinase (MAPK) family, p38γ involved in ferroptosis various diseases. This study explored how effects chronic EtOH consumption caused cerebral I/R. Brain damage was induced mice via administration liquid alcohol-containing diet for 8 weeks, middle artery occlusion reperfusion (MCAO/R), or combination both. We verified significantly exacerbated MCAO/R-induced damage, inflammation. Notably, levels were increased experimental mouse cell models. knockdown markedly attenuated tissue inflammatory infiltration + MCAO/R-treated mice. Mechanistic experiments revealed regulate through p53/SLC7A11 pathway. Overall, our results indicate crucial regulating EtOH- I/R-induced modulating

Language: Английский

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