2020
Yiru Wang, Qingyun Jia, Yifan Zhang, Jing Wei, and Ping Liu
Abstract
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 Tnfα production by immunofluorescence staining. MAPKs, AP-1 and NF-κB p65 pathways were also explored.
Amygdalin decreased body weight, serum lipids, plaque size, lymphatic vessels and inflammatory cytokines (Il-6, Tnfα), Nos1 and Nos2, and increased Il-10 expression in ApoE−/− mice. In oxLDL-induced bone marrow-derived macrophages, amygdalin reduced inflammatory cytokines (Il-6, Tnfα), 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-κB 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-κB p65 signaling pathways in ApoE−/− mice and oxLDL-treated bone marrow-derived macrophages.
