Valproic acid ameliorates cauda equina injury by suppressing HDAC2-mediated ferroptosis.

ABSTRACT:

Introduction

Persistent neuroinflammatory response after cauda equina injury (CEI) lowers nociceptor firing thresholds, accompanied by pathological pain and decreasing extremity dysfunction. Histone deacetylation has been considered a key regulator of immunity, inflammation, and neurological dysfunction. Our previous study suggested that valproic acid (VPA), a histone deacetylase inhibitor, exhibited neuroprotective effects in rat models of CEI, although the underlying mechanism remains elusive.

Methods

The cauda equina compression surgery was performed to establish the CEI model. The Basso, Beattie, Bresnahan score, and the von Frey filament test were carried out to measure the animal behavior. Immunofluorescence staining of myelin basic protein and GPX4 was carried out. In

SUBMITTER: Kong Q 

PROVIDER: S-EPMC11017456 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature