Baicalin protects LPS-induced blood-brain barrier damage and activates Nrf2-mediated antioxidant stress pathway.

The integrity of the BBB is closely related to brain microvascular endothelial cells and TJs, and its dysfunction can lead to stroke, multiple sclerosis, extracranial injury and neurodegenerative diseases. Baicalin is one of the main bioactive extracts from Scutellaria Baicalensis Georgi, which has anti-inflammatory and anti-oxidation pharmacological functions. Preventive protection with baicalin for seven consecutive days can significantly improve the appearance of cell apoptosis and Fluorescein sodium infiltration in the brain tissue of BALB/C mice. In addition, baicalin can inhibit the production of pro-inflammatory cytokines induced by LPS in mice and bEnd.3 cells, including IL-1β and TNF-α. At the same time, LPS caused a decrease in tight junction proteins in the blood-brain barrier, but baicalin can alleviate the damage of the blood-brain barrier by up-regulating Claudin-5 and ZO-1 protein expression. In addition, the results showed that baicalin reduced the production of ROS and MDA in bEnd.3 cells and promoted the production of SOD, and up-regulated the expression of Nrf2, HO-1 and NQO1. The mechanism of this change was mediated by activating the Nrf2 signaling pathway. All in all, Baicalin protected LPS-induced blood-brain barrier damage and activateed Nrf2-mediated antioxidant stress pathway.