Open AccessThe Potential Dual Effects of Anesthetic Isoflurane on Hypoxia-Induced Caspase-3 Activation and Increases in β-Site Amyloid Precursor Protein-Cleaving Enzyme Levels
Author(s) -
C. Pan,
Zhipeng Xu,
Yuanlin Dong,
Yiying Zhang,
Jun Zhang,
Sayre McAuliffe,
Yun Yue,
Tianzuo Li,
Zhongcong Xie
Publication year - 2011
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/ane.0b013e3182185fee
Subject(s) - neurotoxicity , isoflurane , hypoxia (environmental) , pharmacology , apoptosis , amyloid precursor protein , caspase , caspase 3 , anesthetic , medicine , biochemistry , chemistry , toxicity , alzheimer's disease , anesthesia , programmed cell death , disease , oxygen , organic chemistry
β-Amyloid protein (Aβ) accumulation, caspase activation, apoptosis, and hypoxia-induced neurotoxicity have been suggested to be involved in Alzheimer disease neuropathogenesis. Aβ is produced from amyloid precursor protein through proteolytic processing by the aspartyl protease β-site amyloid precursor protein-cleaving enzyme (BACE) and γ-secretase. Inhaled anesthetics have long been considered to protect against neurotoxicity. However, recent studies have suggested that the inhaled anesthetic isoflurane may promote neurotoxicity by inducing caspase activation and apoptosis, and by increasing levels of BACE and Aβ. We therefore sought to determine whether isoflurane can induce concentration-dependent dual effects on hypoxia-induced caspase-3 activation and increases in BACE levels: protection versus promotion.