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Quercetin Attenuates Decrease of Thioredoxin Expression Following Focal Cerebral Ischemia and Glutamate-induced
Dong-Ju Park1, Ju-Bin Kang1, Fawad-Ali Shah1
1Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 52828, South Korea.
Neuroscience
|December 25, 2019
Summary
Quercetin, a plant flavonoid, protects brain cells from stroke damage by increasing thioredoxin, an antioxidant protein. This study shows quercetin helps maintain thioredoxin levels and its interaction with ASK1, crucial for neuroprotection.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Quercetin is a flavonoid found in plants with known neuroprotective properties.
- Cerebral ischemia, often caused by stroke, leads to significant neuronal damage.
- Thioredoxin is a key antioxidant protein involved in regulating cellular redox balance.
Purpose of the Study:
- To investigate the effect of quercetin on thioredoxin expression in models of focal cerebral ischemia and glutamate-induced neuronal cell death.
- To determine if quercetin's neuroprotective effects are mediated through the regulation of thioredoxin.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in rats to induce focal cerebral ischemia.
- Proteomic analysis, reverse-transcription PCR, and Western blot to assess thioredoxin expression.
- Immunoprecipitation to analyze the interaction between thioredoxin and apoptosis signal-regulating kinase 1 (ASK1).
- In vitro studies using glutamate-treated hippocampal and cortical neuron cultures, including thioredoxin-silenced neurons.
Main Results:
- Quercetin administration alleviated neurological deficits, brain edema, and histopathological damage in MCAO rats.
- Quercetin treatment prevented the decrease in thioredoxin expression and the number of thioredoxin-positive cells observed after MCAO.
- Quercetin maintained the interaction between thioredoxin and ASK1, which was reduced by MCAO.
- In vitro, quercetin improved cell viability and increased thioredoxin expression in glutamate-treated neurons.
- The anti-apoptotic effect of quercetin was diminished in thioredoxin-silenced neurons.
Conclusions:
- Quercetin exerts neuroprotective effects against focal cerebral ischemia and glutamate-induced neuronal damage.
- These protective effects are, at least in part, mediated by the upregulation of thioredoxin expression.
- Quercetin helps maintain the functional interaction between thioredoxin and ASK1, contributing to its antioxidant and anti-apoptotic roles.
