Emodin Promotes Atherosclerotic Plaque Stability in Fat-Fed Apolipoprotein E-Deficient Mice

DOI Web Site 参考文献63件
  • Zhou Mingxue
    China Academy of Chinese Medical Sciences
  • Xu Hao
    National Integrative Medicine Center for Cardiovascular Disease, China-Japan Friendship Hospital
  • Pan Lin
    Institution of Clinical Medical Sciences, China-Japan Friendship Hospital
  • Wen Jianyan
    National Integrative Medicine Center for Cardiovascular Disease, China-Japan Friendship Hospital
  • Guo Yanru
    Institution of Clinical Medical Sciences, China-Japan Friendship Hospital
  • Chen Keji
    National Integrative Medicine Center for Cardiovascular Disease, China-Japan Friendship Hospital Xiyuan Hospital, China Academy of Chinese Medical Sciences

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Increasing evidence indicated that plaque stabilization is attributed to the composition of the atherosclerotic plaque, and inflammation plays an important role in the formation and progress of vulnerable atherosclerotic plaque (VAP), which is prone to rupture. Emodin, an important component of traditional Chinese herb rhubarb, has obvious anti-inflammatory effect, although its effect on atherosclerotic plaque stabilization is unknown. Apolipoprotein E (ApoE) is an important component of plasma lipoprotein with anti-atherosclerosis function, and the plaque in the aorta of ApoE-deficient mice has been demonstrated with characteristics of VAP. Therefore, this study was designed to determine whether emodin can stabilize the VAP in the ApoE-deficient mice and explain the possible mechanism. After fat-fed for 13 weeks, mice were randomized into three groups (11 animals/group) and intragastrically administrated with emodin, simvastatin or distilled water for 13 weeks, respectively. The plaque stability was evaluated by the morphology and composition of atherosclerotic plaques. Additionally, the expression of peroxisomal proliferator-activated receptor-γ (PPAR-γ), granulocyte-macrophage colony-stimulating factor (GM-CSF), and matrix metalloproteinase 9 (MMP-9) in plaques was determined by the immunohistochemistry method. We showed that emodin could decrease the lipid core area and the ratio of lipid to collagen content in plaques. In addition, emodin significantly inhibited the expression of GM-CSF and MMP-9, whereas it induced the expression of PPAR-γ in plaques. In conclusion, these results suggest that emodin can stabilize the VAP in the aortic root of ApoE-knockout mice, which is probably due to its anti-inflammatory effect.

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