Journal of veterinary science · 2025
Baicalin modulates metabolic and inflammatory proteins and attenuates neuronal damage in a rat model of ischemic stroke.
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Son Hyun-Kyoung, Park Dong-Ju, Kim Hun-Hwan, Kang Ju-Bin, Koh Phil-Ok
Аннотация
IMPORTANCE: 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.
OBJECTIVE: To identify proteins regulated by baicalin in a rat model of ischemic stroke.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS AND RELEVANCE: 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.
OBJECTIVE: To identify proteins regulated by baicalin in a rat model of ischemic stroke.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS AND RELEVANCE: 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.