Monoammonium glycyrrhizinate ameliorates mitochondrial dysfunction-mediated oxidative stress and neuroinflammation via the NRF2/NQO1 axis after spinal cord injury.

ABSTRACT:

Background

Spinal cord injury (SCI)-induced mitochondrial dysfunction in microglia exacerbates neuroinflammation and neurological deficits. Monoammonium glycyrrhizinate (MAG), a bioactive liquorice-derived compound, exhibits anti-inflammatory and antioxidant properties; however, its effects on microglial mitochondria remain unknown.

Methods

Mice received a moderate contusion injury at the T10 spinal segment. Histopathology was assessed using Hematoxylin-Eosin, Nissl staining, and Luxol Fast Blue; locomotor recovery was evaluated via the Basso Mouse Scale, hindlimb flexion scoring, and gait footprint analysis. RNA-Seq and molecular docking identified KEAP1/NRF2 signaling. Verification employed qPCR, Western blot, and immunofluorescence. Mitochondrial function was gauged by JC

SUBMITTER: Wang T 

PROVIDER: S-EPMC12621352 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature