Related Experiment Video For Actue carbon monoxide poisoning
Updated: Feb 15, 2026

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
Published on: November 19, 2008
iTRAQ-based differential proteomic analysis of the brains in a rat model of delayedcarbon monoxide encephalopathy
Peng Zhang1, Yalei Dai1, Jincheng Xiong2
1Department of Forensic Medicine, Faculty of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, China.
Abstract:
Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a difficult-to-manage neurological complication that can severely affect the life quality of patients. Although the central nervous system (CNS) injuries have been reported, the underlying molecular mechanisms are still unclear. Therefore, we established a rat model of DEACMP, applying isobaric tags for a relative and absolute quantification (iTRAQ)-based proteomics approach to identify differentially expressed proteins in cerebral tissue. A total of 170 proteins in the CO exposure groups were identified as differentially changed. Bioinformatics analysis suggested that these proteins are mainly involved in the biological processes, such as energy metabolism and many neurodegenerative diseases. Three proteins, Glial fibrillary acidic protein (GFAP), mitochondrial malate dehydrogenase (MDHM), and isocitrate dehydrogenase [NAD] subunit alpha (IDH3A), were identified as playing important roles in CNS injuries in DEACMP, and were successfully confirmed by immunohistochemistry analysis. Our study not only offers us new insights into the pathophysiological mechanisms of CNS injuries in DEACMP, but also may provide clinicians with important references in early prevention and treatment.
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