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Monitoring Astrocyte Reactivity and Proliferation in Vitro Under Ischemic-Like Conditions
Published on: October 21, 2017
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Decitabine attenuates ischemic stroke by reducing astrocytes proliferation in rats
Qi Zhang1, Dan Li1, Haihua Zhao1
1Department of Human Anatomy, College of Basic Medical Sciences, China Medical University, Shenyang, China.
Plos One
|August 2, 2022
Summary
Decitabine reduces brain damage in ischemic stroke by inhibiting DNA methylation. This epigenetic regulation lowers astrocyte proliferation and neuronal death, decreasing infarct volume.
Area of Science:
- Neuroscience
- Epigenetics
- Pharmacology
Background:
- DNA methylation is a key epigenetic mechanism regulating gene expression in ischemic stroke.
- Decitabine, a DNA methylation inhibitor, shows therapeutic potential but its mechanism in stroke is unclear.
Purpose of the Study:
- To elucidate the mechanism by which decitabine attenuates ischemic stroke.
- To investigate the effect of decitabine on DNA methylation, astrocyte proliferation, and neuronal survival.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in Sprague-Dawley rats.
- Treatment with decitabine or vehicle, followed by assessment of DNA methylation, infarct volume, astrocyte proliferation, and CDKN1B (p27) expression.
Main Results:
- Decitabine treatment led to hypomethylation and reduced infarct volume in the cortex.
- Decitabine decreased DNA methylation in astrocytes, upregulated p27 mRNA and protein, and attenuated astrocyte proliferation.
- These effects were observed both in vivo and in vitro.
Conclusions:
- Decitabine promotes p27 gene expression, potentially by inhibiting its DNA methylation.
- This mechanism reduces astrocyte proliferation, neuronal death, and infarct volume following ischemic stroke.
