Cerebral ischemia is a serious neurological disorder that can lead to high morbidity and mortality. Baicalin is a naturally bioactive flavonoid derived from Scutellaria baicalensis Georgi, which has neuroprotective activity. Baicalin exerts a neuroprotective effect against hypoxic ischemic injury. In this study, we investigated whether baicalin regulates specific proteins in the cerebral cortex of ischemic stroke animals. Middle cerebral artery occlusion (MCAO) surgery was performed to induce ischemic brain injury, and baicalin (30 mg/kg) or vehicle was injected into the abdominal cavity before MCAO surgery. Neurological behavior tests were performed 24 h after MCAO surgery and proteomics approach was performed using proteins extracted from cortical tissue. Two-dimensional electrophoresis analysis and MALDI-TOF were performed to identify the regulated protein by baicalin. MCAO damage caused severe behavioral disorders, but baicalin treatment improved these behavioral deficits. Baicalin also induced changes in the expression of various proteins in the cerebral cortex of MCAO animals. Proteins changed by baicalin administration are as follow: adenosylhomocysteinase, isocitrate dehydrogenase [NAD] subunit alpha, apolipoprotein A-I, Rab GDP dissociation inhibitor beta, eukaryotic initiation factor 4A, and mu-crystallin. These proteins were involved in metabolism and protein synthesis. The results of this study demonstrated the neuroprotective effects of baicalin by improving behavioral disorders caused by MCAO damage. The results also showed that baicalin regulates the expression of a variety of proteins involved in neuroprotective functions. Therefore, our findings provide evidence that baicalin plays a neuroprotective role in stroke animal models by regulating specific proteins.

Ischemic stroke causes brain damage and neuronal cell death by depriving oxygen and nutrients and releasing excessive levels of glutamate and intracellular calcium. Epigallocatechin gallate (EGCG) is a polyphenolic compound present in green tea. It has antioxidant, anti-inflammatory, and neuroprotective effects. Hippocalcin is a calcium binding protein that regulates calcium concentration, neuronal differentiation, neuronal excitability, and neuronal cell death. In this study, we investigated whether EGCG regulates the expression of hippocalcin in neurons and astrocytes after focal cerebral ischemia. Cerebral ischemia was induced by meddle cerebral artery occlusion (MCAO). EGCG (50 mg/kg) or PBS was injected into the abdominal cavity just before MCAO surgery. Neurobehavioral tests were performed to evaluate the effect of EGCG on neurological behavioral deficits 24 h after MCAO surgery. Immunofluorescence staining was performed to evaluate the positive response to hippocalcin in the cerebral cortex after MCAO surgery. We also detected the positive reactions of neuronal nuclear protein (NeuN) and glial fibrillary acidic protein (GFAP) as markers of neuron and astrocyte, respectively. MCAO caused severe neurological impairment and EGCG treatment attenuated these impairments. MCAO damage reduced the number of NeuN-positive cells and increased the number of GFAP-positive cells. This result indicates a decrease in neurons and an increase in astrocytes. However, EGCG alleviated these changes caused by MCAO damage. MCAO reduced the number of hippocalcin-positive cells in neurons and astrocytes, and EGCG treatment attenuated these reductions. Hippocalcin exerts neuroprotective effect through regulating intracellular calcium concentration. In conclusion, EGCG regulates the expression of hippocalcin in neurons and astrocytes and has neuroprotective effects in focal cerebral ischemia.