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Ginsenoside Rb1 Enhances Plaque Stability and Inhibits Adventitial Vasa Vasorum via the Modulation of miR-33 and PEDF
Xiaoyan Yang1,2, Lei Wang1, Zihao Zhang1
1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China.
Ginsenoside Rb1 stabilizes atherosclerotic plaques by inhibiting adventitial vasa vasorum (VV) growth and inflammation. This effect is mediated by modulating miR-33 and Pigment epithelium-derived factor (PEDF).
Area of Science:
- Cardiovascular Research
- Pharmacology
- Molecular Biology
Background:
- Atherosclerosis progression is linked to adventitial vasa vasorum (VV) proliferation, increasing plaque vulnerability.
- Understanding factors that stabilize atherosclerotic plaques is crucial for disease management.
Purpose of the Study:
- To investigate the effects of Ginsenoside Rb1 (Rb1) on atherosclerotic plaque stabilization and adventitial VV.
- To elucidate the underlying molecular mechanisms involving miR-33 and Pigment epithelium-derived factor (PEDF).
Main Methods:
- Apolipoprotein E-deficient (ApoE-/-) mice were fed a high-fat diet and treated with Rb1.
- Adventitial VV proliferation, inflammation, plaque burden, and stability were assessed.
- The role of miR-33 and PEDF in mediating Rb1's effects was analyzed.
Main Results:
- Rb1 treatment significantly inhibited adventitial VV proliferation, reduced inflammation, and decreased plaque burden in ApoE-/- mice.
- Rb1 treatment stabilized atherosclerotic plaques, an effect attenuated by miR-33 overexpression.
- Rb1 induced Pigment epithelium-derived factor (PEDF) expression and reduced miR-33 generation.
Conclusions:
- Ginsenoside Rb1 attenuates atherosclerotic plaque growth and enhances stability by inhibiting adventitial VV proliferation and inflammation.
- The anti-angiogenic and anti-inflammatory effects of Rb1 are mediated through the modulation of miR-33 and its target gene PEDF.
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