Baicalin alleviates atherosclerosis by relieving oxidative stress and inflammatory responses via inactivating the NF-κB and p38 MAPK signaling pathways.

Atherosclerosis (AS) is a chronic progressive disease related to inflammatory reaction. Baicalin is a flavonoid isolated from Scutellaria baicalensis georgi (Huang-qin) and exerts anti-inflammation effects in various diseases. Here, we investigated the protective effects of baicalin treatment and the potential mechanism in AS progression on AS mouse model. After ApoE-/- mice with high-lipid diets had received 12 weeks' of baicalin treatment at different concentrations, plasma lipids levels and atherosclerotic plaque areas in aorta were measured and there exhibited a prominent improvement in the baicalin treated mice compared with mice in AS model group. The expression of lipolysis related proteins (PPARα, CPT-1) was increased while the expression of adipogenesis related proteins (SREBP-1c, ACS) was decreased by baicalin treatment, indicating the anti-adipogenic effect of baicalin. Moreover, baicalin up-regulated the activities of antioxidant enzymes (SOD, CAT and GSH-Px) and down-regulated the activity of oxidative parameter MDA compared with AS model group, indicating the anti-oxidant effect of baicalin. The increased levels of pro-inflammatory cytokines (IL-6, TNF-α, sVE-cadherin) induced by AS were also decreased by baicalin treatment, indicating that baicalin acted as an anti-inflammation regulator in AS. In addition, we further explored the potential mechanism of baicalin treatment on AS, and found that baicalin treatment attenuated the high phosphorylation levels of JNK, p65, p-38 and ERK1/2 induced by AS, indicating that baicalin treatment inhibited the NF-κB and p38 MAPK signaling pathways in AS. In conclusion, baicalin treatment inhibited the NF-κB and p38 MAPK signaling pathways, thereby achieved its anti-adipogenic effect, anti-oxidant effect and anti-inflammation effect in a dose-dependent manner in AS.