ETHNOPHARMACOLOGICAL RELEVANCE: Baicalin is one of the principal flavonoids isolated from the dried root of Scutellariae Baicalensis Georgi and has been widely used as a traditional herbal medicine to suppress brain edema and reduce cerebral ischemic damage. However, the effects of baicalin on the blood-brain barrier (BBB) are poorly understood. AIM OF THE STUDY: To explore the effects of baicalin on the permeability of the BBB under ischemic conditions in vitro with regard to changes in the tight junctions(TJ) proteins claudin-5 and zonula occludens-1 (ZO-1). MATERIALS AND METHODS: Brain microvascular endothelial cells(BMVECs) from Bal b/c mice were cultured to establish an in vitro BBB model. Oxygen and glucose deprivation (OGD) was applied to simulate ischemia. The experiment consisted of a normal control group, a model group and baicalin-treated groups (high-dose group, moderate-dose group and low-dose group). Transendothelial electrical resistance (TEER) and permeability to HRP were used as indicators of changes in BBB permeability. A real-time fluorescent quantitative assay was utilized to monitor the transcriptional changes in claudin-5 and ZO-1, and western blotting was used to detect the changes in protein expression of claudin-5, ZO-1 and PKC. RESULTS: OGD led to a significant increase of permeability in this in vitro BBB model. Baicalin effectively decreased the permeability of the BBB, promoted transcription and expression of TJ proteins (claudin-5 and ZO-1) and reduced the levels of PKC. CONCLUSIONS: We propose that baicalin is capable of restoring the barrier function of the BBB under ischemic conditions and this beneficial effect may be linked to the decreased expression of TJ proteins.
ETHNOPHARMACOLOGICAL RELEVANCE: Baicalin is one of the principal flavonoids isolated from the dried root of Scutellariae Baicalensis Georgi and has been widely used as a traditional herbal medicine to suppress brain edema and reduce cerebral ischemic damage. However, the effects of baicalin on the blood-brain barrier (BBB) are poorly understood. AIM OF THE STUDY: To explore the effects of baicalin on the permeability of the BBB under ischemic conditions in vitro with regard to changes in the tight junctions(TJ) proteins claudin-5 and zonula occludens-1 (ZO-1). MATERIALS AND METHODS: Brain microvascular endothelial cells(BMVECs) from Bal b/c mice were cultured to establish an in vitro BBB model. Oxygen and glucose deprivation (OGD) was applied to simulate ischemia. The experiment consisted of a normal control group, a model group and baicalin-treated groups (high-dose group, moderate-dose group and low-dose group). Transendothelial electrical resistance (TEER) and permeability to HRP were used as indicators of changes in BBB permeability. A real-time fluorescent quantitative assay was utilized to monitor the transcriptional changes in claudin-5 and ZO-1, and western blotting was used to detect the changes in protein expression of claudin-5, ZO-1 and PKC. RESULTS:OGD led to a significant increase of permeability in this in vitro BBB model. Baicalin effectively decreased the permeability of the BBB, promoted transcription and expression of TJ proteins (claudin-5 and ZO-1) and reduced the levels of PKC. CONCLUSIONS: We propose that baicalin is capable of restoring the barrier function of the BBB under ischemic conditions and this beneficial effect may be linked to the decreased expression of TJ proteins.