Baicalin modulates metabolic and inflammatory proteins and attenuates neuronal damage in a rat model of ischemic...

Cerebral ischemia arises from insufficient blood flow to the brain, resulting in substantial metabolic disturbances. Baicalin, a flavonoid compound derived from Scutellaria baicalensis, has anti-inflammatory, antioxidant, and neuroprotective properties.

To identify proteins regulated by baicalin in a rat model of ischemic stroke.

Adult male Sprague Dawley rats underwent middle cerebral artery occlusion (MCAO) or sham surgery and received intraperitoneal baicalin (100 mg/kg) or vehicle 1 h before surgery. Neurobehavioral assessments were performed 24 h after MCAO, and cerebral cortex tissues were collected. Cortical damage was evaluated using 2,3,5-triphenyltetrazolium chloride staining and hematoxylin-eosin staining. Protein expression changes between groups were assessed by liquid chromatography-tandem mass spectrometry, and selected targets were validated by reverse transcription-polymerase chain reaction.

MCAO induced marked neurological deficits, infarction, and histopathological damage, all of which were significantly attenuated by baicalin treatment. MCAO decreased adenylate cyclase type 1 and solute carrier family 25 member 12 levels, and baicalin mitigated these reductions. Baicalin also reduced MCAO-induced increases in C-reactive protein and apolipoprotein C-II, as well as alpha-1 microglobulin, murinoglobulin, and hemoglobin subunit B, proteins associated with inflammation, lipid metabolism, mitochondrial function, and cellular injury.

Baicalin exerts neuroprotective effects in cerebral ischemia by modulating proteins involved in energy metabolism, myelination, and neuroinflammation. These findings support baicalin as a promising therapeutic candidate in experimental stroke models.