Amyloid Beta-Induced Mitochondrial Dysfunction and Endothelial Permeability in Cerebral Microvascular Endothelial cells: the protective role of Dexmedetomidine. DOI Creative Commons
Haifeng Zhao, Mingyue Fan, Jin Zhang

et al.

Brain Research Bulletin, Journal Year: 2024, Volume and Issue: 220, P. 111137 - 111137

Published: Nov. 20, 2024

Postoperative cognitive dysfunction (POCD) is a common complication in patients who undergo anesthesia different types of surgeries. Emerging evidence implicates elevated beta-amyloid (Aβ) the pathogenesis POCD. Meanwhile, Dexmedetomidine (DEX) has recently shown promise reducing POCD incidence. This study aimed to elucidate role Aβ inducing endothelial permeability cerebral microvascular cells and underlying mechanisms testing effects DEX. We demonstrated that Aβ1-42, prevalent form related POCD, cytotoxic HBMECs, increasing transendothelial mitochondrial dysfunction, as evidenced by reactive oxygen species (ROS) decreased ATP production membrane potential. Furthermore, Aβ1-42 was inhibit Sirt3, exacerbating dysfunction. Conversely, DEX found prevent Aβ1-42-induced increases preserved tight junction proteins HBMECs.These findings suggest DEX, Sirt3 activator, may offer pharmacological strategy mitigate Aβ1-42-related cell preserve function post-surgery.

Language: Английский

Roles of SIRT3 in cardiovascular and neurodegenerative diseases DOI
Liang Chen, Anqi Zhao, Ying Li

et al.

Ageing Research Reviews, Journal Year: 2025, Volume and Issue: unknown, P. 102654 - 102654

Published: Jan. 1, 2025

Language: Английский

Citations

1
Amyloid Beta-Induced Mitochondrial Dysfunction and Endothelial Permeability in Cerebral Microvascular Endothelial cells: the protective role of Dexmedetomidine. DOI Creative Commons
Haifeng Zhao, Mingyue Fan, Jin Zhang

et al.

Brain Research Bulletin, Journal Year: 2024, Volume and Issue: 220, P. 111137 - 111137

Published: Nov. 20, 2024

Postoperative cognitive dysfunction (POCD) is a common complication in patients who undergo anesthesia different types of surgeries. Emerging evidence implicates elevated beta-amyloid (Aβ) the pathogenesis POCD. Meanwhile, Dexmedetomidine (DEX) has recently shown promise reducing POCD incidence. This study aimed to elucidate role Aβ inducing endothelial permeability cerebral microvascular cells and underlying mechanisms testing effects DEX. We demonstrated that Aβ1-42, prevalent form related POCD, cytotoxic HBMECs, increasing transendothelial mitochondrial dysfunction, as evidenced by reactive oxygen species (ROS) decreased ATP production membrane potential. Furthermore, Aβ1-42 was inhibit Sirt3, exacerbating dysfunction. Conversely, DEX found prevent Aβ1-42-induced increases preserved tight junction proteins HBMECs.These findings suggest DEX, Sirt3 activator, may offer pharmacological strategy mitigate Aβ1-42-related cell preserve function post-surgery.

Language: Английский

Citations

0