Isoliquiritigenin regulates microglial M1/M2 polarisation by mediating the P38/MAPK pathway in cerebral stroke.

The article investigates the effects of isoliquiritigenin (ILG), a flavonoid derived from Glycyrrhizae Rhizoma, on microglial polarization and brain injury in ischemic stroke. Using a transient middle cerebral artery occlusion (tMCAO) rat model and lipopolysaccharide (LPS)-induced BV2 microglial cells, the study demonstrates that ILG reduces infarct volume and neurological deficits by promoting the anti-inflammatory M2 microglial phenotype while suppressing the pro-inflammatory M1 phenotype. Mechanistically, ILG inhibits activation of the p38 mitogen-activated protein kinase (p38/MAPK) signaling pathway, and modulation of this pathway reverses or enhances ILG’s effects on microglial polarization. These findings suggest that ILG’s neuroprotective role in ischemic stroke involves regulation of microglial polarization via inactivation of the p38/MAPK pathway, highlighting its potential as a therapeutic agent for ischemic stroke.