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Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
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Aged garlic extract suppresses inflammation in apolipoprotein E-knockout mice.
Naoaki Morihara1, Atsuko Hino2, Satomi Miki1
1Drug Discovery Laboratory, Wakunaga Pharmaceutical Co., Ltd., Hiroshima, Japan.
Molecular Nutrition & Food Research
|July 21, 2017
Summary
Aged garlic extract (AGE) significantly reduces atherosclerosis progression in mice by suppressing key inflammatory markers. This study highlights AGE
Area of Science:
- Cardiovascular Research
- Inflammation Biology
- Nutraceutical Science
Background:
- Chronic inflammation is a key driver in the development and advancement of atherosclerotic plaques.
- Understanding the mechanisms by which natural compounds affect atherosclerosis is crucial for developing preventative strategies.
Purpose of the Study:
- To investigate the anti-inflammatory effects of aged garlic extract (AGE) in a mouse model of atherosclerosis.
- To elucidate the molecular pathways through which AGE may retard the progression of atherosclerotic lesions.
Main Methods:
- Apolipoprotein E-knockout (ApoE-KO) mice were administered a standard diet with or without 3% aged garlic extract (AGE) for 12 weeks.
- Measurements included atherosclerotic lesion progression, serum levels of C-reactive protein (CRP) and thromboxane B2 (TXB2), and hepatic levels of tumor necrosis factor alpha (TNF-α), interleukin-1 receptor-associated kinase 4 (IRAK4), and phospho-AMP-activated protein kinase (p-AMPK).
Main Results:
- AGE administration inhibited atherosclerotic lesion progression by 27%.
- Serum levels of CRP and TXB2 were reduced by 39% and 33%, respectively.
- Hepatic levels of TNF-α and IRAK4 decreased by 35% and 60%, respectively, while phospho-AMPK levels doubled.
Conclusions:
- The anti-atherosclerotic effect of AGE is mediated through the suppression of inflammatory pathways.
- AGE reduces key inflammatory markers (CRP, TXB2, TNF-α, IRAK4) and enhances AMPK activity in the liver.
- These findings suggest AGE as a potential therapeutic agent for mitigating atherosclerosis.

