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 100. μM (high dose) and 10. μM (low dose) for 6. h after a 2. h 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-k{cyrillic}B signaling pathway such as p-IKKα, p-IKKβ and p-IκBα. Furthermore, baicalin at 10. μM 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.