Baicalin protects rat brain microvascular endothelial cells injured by oxygen-glucose deprivation via anti-inflammation.

Baicalin, which is isolated from Scutellariae Radix, has been evidenced to possess several pharmacological effects. The present study focuses on the in vitro protective effect of baicalin on oxygen-glucose deprivation (OGD) injured brain microvascular endothelial cells (BMECs) via anti-inflammation and mechanisms against BMECs damaged by OGD. Cultured primary rat BMECs were exposed to baicalin at the concentrations of 100μM (high dose) and 10μM (low dose) for 6h after a 2h OGD. The effects of baicalin were evaluated in terms of (i) cell viability; (ii) lactate dehydrogenase (LDH) leakage rate; (iii) levels of TNF-α, IL-1β, IL-6 in culture media; (iv) protein expressions of p-MEK6, p-MEK1/2, p-ERK, p-IκBα, NF-κB p65, p-IKKα, p-IKKβ and p-p38; and (v) nuclear translocation of NF-κB p65 and p-IκBα. The results showed that OGD treatment could reduce cell viability, increase LDH leakage rate, increase the levels of TNF-α, IL-1β and IL-6 in the culture media. These effects were suppressed by baicalin with high or low dose. In addition, baicalin could notably down-regulate the phosphorylation of proteins in MAPK signaling pathway such as p-MRK1/2, p-ERK and p-p38. While low dose of baicalin could significantly suppress the phosphorylation of proteins in NF-кB signaling pathway such as p-IKKα, p-IKKβ and p-IκBα. Furthermore, baicalin at 10μM could remarkably inhibit nuclear transcriptional activity triggered via NF-κB p65 and p-IκBα in BMECs. In conclusion, baicalin displays a protective effect on OGD-injured BMECs in vitro by attenuating inflammatory factors via down-regulated the MAPK and NF-κB signaling pathway.