Amygdalin Attenuates Atherosclerosis and Plays an Anti-Inflammatory Role in ApoE Knock-Out Mice and Bone Marrow-Derived Macrophages

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.

Qianjinweijing Decoction Protects Against Fine Particulate Matter Exposure-mediated Lung Function Disorder

“…According to MS spectrum and retention times of UPLC-Q-TOF/MS analysis, peaks of QJWJ were tentatively identified as Coixol (Supplementary Figure S2), Asperglaucide (Supplementary Figure S3), and Amygdalin (Supplementary Figure S4) in negative ion mode, Tricin (Supplementary Figure S5) in positive ion mode. Taken together, the major chemical active components of QJWJ were Coixol, Asperglaucide, Amygdalin, and Tricinj, which were consistent with previous studies (Gao et al, 2009;Fan et al, 2015;Wang et al, 2020;Li et al, 2021).…”

Guanxinkang Decoction Attenuates the Inflammation in Atherosclerosis by Regulating Efferocytosis and MAPKs Signaling Pathway in LDLR−/− Mice and RAW264.7 Cells

“…Recent studies have shown that MAPKs signaling pathway is activated to attenuate inflammation in AS ( Wang et al, 2020a ; Wang et al, 2020b ; Lu et al, 2020 ), making MAPKs an ideal target of drug therapy. NF-κB, a critical transcription factor in inflammatory responses, can be activated by ox-LDL to promote AS ( Chávez-Sánchez et al, 2010 ).…”

Transcriptome profiling reveals new insights into the roles of neuronal nitric oxide synthase on macrophage polarization towards classically activated phenotype

“…Further, NOS1 also regulates dendritic cell maturation in humans and is required for iNOS expression in allergen-induced asthma in mice [ 10 , 11 ]. In oxidized low-density lipoprotein (oxLDL)-induced bone marrow-derived macrophages (BMDMs), the levels of inflammatory cytokines IL6 and TNFα were associated with NOS1 expression [ 12 ]. In addition, inflammation can be promoted by NOS1-synthesized NO at lower concentrations [ 13 , 14 ].…”