Baicalin reduces the permeability of the blood-brain barrier during hypoxia in vitro by increasing the expression of tight junction proteins in brain microvascular endothelial cells.

Background: 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.

Objective: 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).

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.