HDAC1 dysregulation promotes pro-inflammatory microglial activation and aggravates post-stroke neuroinflammation.

ABSTRACT:

Background

Histone deacetylase 1 (HDAC1) is a key epigenetic regulator involved in DNA repair and neuronal survival. While HDAC1 downregulation has been implicated in ischemic brain injury, its role in regulating microglial functional shift and neuroinflammation remains unclear. This study aimed to investigate how HDAC1 dysfunction influences microglial activation states and contributes to neuroinflammatory processes in ischemic stroke.

Methods

Using a rat model of endothelin-1-induced focal cerebral ischemia, HDAC1 knockdown was achieved via stereotactic co-injection of HDAC1 siRNA. Immunofluorescence, Western blotting, ELISA, and oxidative stress assays were performed to assess neuroinflammation, microglial polarization, and related signalling pathways. In parallel,

SUBMITTER: Chen JS 

PROVIDER: S-EPMC12704127 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature