Amygdalin ameliorates the progression of atherosclerosis in LDL receptor-deficient mice

Abstract

Previous studies have demonstrated that regulatory T cells (Tregs) are pivotal in the regulation of T cell-mediated immune responses in atherosclerosis, a chronic autoimmune-like disease. In the authors' previous studies, it was demonstrated that amygdalin ameliorated atherosclerosis by the regulation of Tregs in apolipoprotein E-deficient (ApoE−/−) mice. Therefore, the aim of the present study was to investigate the therapeutic effect of amygdalin on low-density lipoprotein (LDL) receptor deficient (LDLR−/−) mice, and to examine its immune regulatory function by the stimulation of Tregs. To establish an atherosclerosis mouse model, the LDLR−/− mice were fed a high fat and high cholesterol diet then the total plasma cholesterol, triglyceride, LDL and chemokines levels were measured by an ELISA. Following sacrificing the mice, the upper sections of the aorta were stained by hematoxylin and eosin, and Oil red O to assess the plaque area. Then western blotting and reverse transcription polymerase chain reactions were performed to analysis the expression levels of cluster of differentiation 68, monocyte chemoattractant protein-1, matrix metalloproteinase (MMP)-2, MMP-9 and forkhead box P3 (Foxp3). To further confirm the activation of FOXP3 by amygdalin, lentiviruses carrying Foxp3 shRNA were injected into the mice, and the serum cytokines levels were measured by ELISA. Following feeding of the mice with a high-fat/high-cholesterol diet, the LDLR−/− mice demonstrated comparatively higher levels of triglyceride, total cholesterol and LDL, compared with levels in the amygdalin-treated mice. By comparing the vessel area, lumen area, plaque area, and percentage aortic plaque coverage, the effects of amygdalin on pre-existing lesions were assessed. In addition, the levels of CD68, monocyte chemoattractant protein-1, MMP-2 and MMP-9 were analyzed, and analysis of the expression of interleukin (IL)-1β, IL-6 and tumor necrosis factor (TNF)-α indicated that the mice treated with amygdalin had decreased expression of pro-inflammatory cytokines. The mRNA and protein levels of Foxp3 were also quantified, and the mice treated with amygdalin demonstrated an increased number of Tregs. The knockdown of Foxp3mRNA resulted in the increased secretion of IL-1β, IL-6 and TNF-α. Therefore, the data indicated that amygdalin regulated the formation of atherosclerosis and stabilized the plaque by suppressing inflammatory responses and promoting the immune-modulation function of Tregs. Taken together, the results demonstrated the therapeutic effect of amygdalin on atherosclerosis.

In silico authentication of amygdalin as a potent anticancer compound in the bitter kernels of family Rosaceae

“…Amygdalin, which is also known as vitamin B17 or Laetrile ( Lv et al, 2017 ), is an aromatic cyanogenic compound that belongs to sub-class of carbohydrates and carbohydrate conjugates. Chemical formula of amygdalin is C 20 H 27 NO 11, having molecular weight of 457.432 g/mol and D-mandelonitrile-beta-D-gentiobioside structure ( Chang et al, 2006 ), as shown in Fig.…”

Fatty Acid Composition and Applications of <i>Eriobotrya japonica</i> Seed Oil

“…In addition, because the acid value of the oil was 50.6 KOH mg/g, the oil was determined to be unsuitable as food 15 . In addition, loquat seed contains amygdalin 4 , and is also known to be unsuitable as food for this reason. Therefore, hexane was used to extract the loquat seed oil.…”

“…Loquat seeds are further used as a traditional medicine to treat cough and indigestion 2 . Amygdalin has been extensively studied as one of the primary active ingredients responsible for these pharmacological effects 4 . In addition to amygdalin, numerous studies have been conducted on other ingredients derived from loquat seeds, and their physiological effects have been elucidated 5 8 .…”

The Signaling Pathways Involved in the Antiatherosclerotic Effects Produced by Chinese Herbal Medicines

“…Moreover, one property of baicalin and geniposide ameliorating AS is ascribed to the gathering blockade of DCs in plaque areas that launch proatherogenic immune reactions [ 146 ]. Owing that regulatory T cells (Tregs) hinder T helper (Th) cells-induced inflammation, QSYQ and amygdalin increase the content of Tregs in vascular lesions which delay the development of AS [ 30 , 147 ]. Additionally, QSYQ directly inhibit Th17 cells in AS areas and then lower the release of IL-17, a proatherogenic cytokine [ 30 ].…”