Ascorbic acid (AA) is significant in protecting the brain from further damage and maintaining brain homeostasis after ischemia stroke (IS); however, the dynamic change of cerebral AA content after different degrees of ischemic stroke is still unclear. Herein, carboxylated single-walled carbon nanotube (CNT -COOH )- and polyethylenedioxythiophene (PEDOT)-modified carbon fiber microelectrodes (CFEs) were proposed to detect in situ cerebral AA with sensitivity, selectivity, and stability. Under differential pulse voltammetry scanning, the CFE/CNT -COOH /PEDOT gave a ratiometric, electrochemically responsive signal. The internal standard peak at -310 mV was from the reversible peak of O 2 reduction and the deprotonation and protonation of quinone groups, while AA was oxidized at -70 mV. In vivo experimental results indicated that the cerebral AA level gradually increased with the ischemic time increasing in different middle cerebral artery occlusion (MCAO) model mice. This work implies that the increasing cerebral AA level may be highly related to the glutamate excitotoxicity and ROS-led cell apoptosis and paves a new way for further understanding the release and metabolic mechanisms of AA during ischemia reperfusion and IS.
Keyphrases
- cerebral ischemia
- subarachnoid hemorrhage
- middle cerebral artery
- brain injury
- carbon nanotubes
- atrial fibrillation
- blood brain barrier
- white matter
- quantum dots
- blood pressure
- living cells
- hydrogen peroxide
- resting state
- dna damage
- type diabetes
- cerebral blood flow
- oxidative stress
- nitric oxide
- adipose tissue
- metabolic syndrome
- ischemia reperfusion injury
- reactive oxygen species
- mass spectrometry
- insulin resistance
- solid phase extraction
- liquid chromatography