<p>This study explores the molecular mechanisms of Yixin Tongbi Formula (YTF) in intervening in atherosclerotic plaques. Thirty-six healthy SD rats were randomly divided into six groups: normal control, model control, low-dose YTF, medium-dose YTF, high-dose YTF, and Atorvastatin groups, with six rats in each. All groups, except for the normal control, were administered a high-fat diet mixed with Vitamin D3 to establish an atherosclerosis (AS) model. After successful model establishment, confirmed by sampling three rats, the treatment groups were administered 10&#xa0;g/kg, 20&#xa0;g/kg, and 40&#xa0;g/kg of YTF, respectively, and the Atorvastatin group received 5&#xa0;mg/kg of Atorvastatin, all once daily for 14 consecutive days. Compared to the normal control group, the model control group showed significant thickening of the aortic walls, and increased levels of TC, TG, HDL, and LDL in serum, as well as elevated levels of MMP-2, MMP-9, IL-6, TNF-α, and ICAM-1 in aortic tissues. Expression of Bax in myocardial tissue increased, while Bcl-2 decreased. These changes were completely reversed by treatment with YTF, with the high-dose group showing the most significant effects. YTF inhibits the development of AS by suppressing inflammation and cell apoptosis and improving plaque stability.</p>

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Yixin Tongbi formula as a therapeutic approach for atherosclerosis by targeting inflammatory mediators and metalloproteinases

  • Qian Nie,
  • Haseeb Sattar,
  • Tao Leng,
  • Rui Wang,
  • Ailing Huang,
  • Xie Wen

摘要

This study explores the molecular mechanisms of Yixin Tongbi Formula (YTF) in intervening in atherosclerotic plaques. Thirty-six healthy SD rats were randomly divided into six groups: normal control, model control, low-dose YTF, medium-dose YTF, high-dose YTF, and Atorvastatin groups, with six rats in each. All groups, except for the normal control, were administered a high-fat diet mixed with Vitamin D3 to establish an atherosclerosis (AS) model. After successful model establishment, confirmed by sampling three rats, the treatment groups were administered 10 g/kg, 20 g/kg, and 40 g/kg of YTF, respectively, and the Atorvastatin group received 5 mg/kg of Atorvastatin, all once daily for 14 consecutive days. Compared to the normal control group, the model control group showed significant thickening of the aortic walls, and increased levels of TC, TG, HDL, and LDL in serum, as well as elevated levels of MMP-2, MMP-9, IL-6, TNF-α, and ICAM-1 in aortic tissues. Expression of Bax in myocardial tissue increased, while Bcl-2 decreased. These changes were completely reversed by treatment with YTF, with the high-dose group showing the most significant effects. YTF inhibits the development of AS by suppressing inflammation and cell apoptosis and improving plaque stability.