Amygdalin Attenuates Atherosclerosis And Plays An Anti-Inflammatory Role In Apoe Knock-Out Mice And Bone Marrow-Derived Macrophages

Amygdalin, the main component of Prunus persica (L.) Stokes, has been used to treat atherosclerosis in mouse model due to its anti-inflammatory role. However, the underlying mechanism remains poorly understood. This study aimed to evidence the influence of amygdalin on high-fat diet-induced atherosclerosis in ApoE knock-out (ApoE(-/-)) mice, and unravel its anti-inflammatory mechanism. ApoE(-/-) mice fed with high-fat diet for eight weeks were randomly divided into four groups and injected with amygdalin at the concentration of 0.08 or 0.04 mg/kg for 12 weeks. Additionally, bone marrow-derived macrophages were intervened with oxidized low-density lipoprotein (oxLDL) or lipopolysaccharide plus various concentrations of amygdalin for further exploration. Body weight, serum lipid profiles and inflammatory cytokines were detected by ELISA, gene expression by RT-PCR, plaque sizes by Oil Red O, lymphatic vessels of heart atrium and Tnf alpha production by immunofluorescence staining. MAPKs, AP-1 and NF-kappa B p65 pathways were also explored. Amygdalin decreased body weight, serum lipids, plaque size, lymphatic vessels and inflammatory cytokines (Il-6, Tnf alpha), Nos1 and Nos2, and increased Il-10 expression in ApoE(-/-) mice. In oxLDL-induced bone marrow-derived macrophages, amygdalin reduced inflammatory cytokines (Il-6, Tnf alpha), Nos1 and Nos2, and increased Il-10 production. These effects were associated with the decreased phosphorylation of Mapk1, Mapk8, Mapk14, Fos and Jun, and the translocation of NF-kappa B p65 from nucleus to cytoplasm. The results suggested that amygdalin could attenuate atherosclerosis and play an anti-inflammatory role via MAPKs, AP-1 and NF-kappa B p65 signaling pathways in ApoE(-/-) mice and oxLDL-treated bone marrow-derived macrophages.