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

• DOI: 10.3892/mmr.2017.7609
• Publication Date: 2017-09-25T11:38:42Z
• Authors: Jianzhen Lv; Wen Xiong; Tiantian Lei; Hailian Wang; Minghan Sun; Erwei Hao; Zhiping Wang; Xiaoqi Huang; Shaoping Deng; Jiagang Deng; Yi Wang
• Keywords: Oil Red O

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