Salvianolic acid B attenuates the inflammatory response in atherosclerosis by regulating MAPKs/ NF-κB signaling pathways in LDLR-/- mice and RAW264.7 cells.

Salvianolic acid B (Sal B) is the main effective water-soluble component of . In this study, the anti-inflammatory effect of Sal B was explored in high-fat-diet (HFD)-induced LDLR-/- mice and oxidized low-density-lipoprotein (ox-LDL)-induced or lipopolysaccharide (LPS)-induced RAW264.7 cells. The LDLR-/- mice were randomly divided into four groups after 12 weeks of high-fat diet. Then, the mice were administrated with 0.9% saline or Sal B (25 mg/kg) or Atorvastatin (1.3 mg/kg) for 12 weeks. RAW 264.7 cells were induced with ox-LDL/LPS, or ox-LDL/LPS plus different concentrations of Sal B (1.25 μg/mL, 2.5 μg/mL, 5 μg/mL), or ox-LDL plus Sal B plus MAPKs activators. ELISA was used for detecting serum lipid profiles and inflammatory cytokines, RT-qPCR used for gene expression, Oil Red O used for plaque sizes, and immunofluorescence staining used for NF-κB p65 and TNF-α production. Inflammation-related proteins and MAPKs pathways were detected by Western Blot. The results showed that Sal B decreased the levels of serum lipids (TC, TG, and LDL-C), attenuated inflammatory cytokines, and improved lipid accumulation in the aorta. Sal B also attenuated the elevation of inflammatory cytokines induced by ox-LDL or LPS in RAW264.7 cells, and the phosphorylation of MAPKs/NF-κB pathways in the aorta and RAW264.7 cells, resulting in a significant decrease in the contents of p-JNK, p-ERK 1/2, p-P38, p-IκB, and p-NF-κB p65. Sal B could exert anti-inflammatory effects on atherosclerosis via MAPKs/NF-κB signaling pathways in vivo and in vitro.