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Aged garlic extract suppresses inflammation in apolipoprotein E‐knockout mice
Author(s) -
Morihara Naoaki,
Hino Atsuko,
Miki Satomi,
Takashima Miyuki,
Suzuki Junichiro
Publication year - 2017
Publication title -
molecular nutrition and food research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.495
H-Index - 131
eISSN - 1613-4133
pISSN - 1613-4125
DOI - 10.1002/mnfr.201700308
Subject(s) - apolipoprotein e , inflammation , medicine , endocrinology , tumor necrosis factor alpha , ampk , apolipoprotein b , c reactive protein , knockout mouse , receptor , immunology , protein kinase a , kinase , biology , cholesterol , biochemistry , disease
Scope Chronic inflammation plays a major role in the formation and progression of atherosclerotic plaques. To clarify the mode of action of aged garlic extract (AGE) to retard atherosclerosis, we investigated whether AGE suppresses the inflammation in apolipoprotein E‐knockout (ApoE‐KO) mice. Methods and results ApoE‐KO mice were fed standard diet with or without 3% AGE for 12 wk. AGE feeding inhibited the progression of atherosclerotic lesion by 27% and reduced the level of C‐reactive protein (CRP) and thromboxane B 2 (TXB 2 ), a marker of platelet activation, in serum by 39 and 33%, respectively, compared to ApoE‐KO mice without AGE treatment. AGE treatment also decreased the level of tumor necrosis factor alpha (TNF‐α), a major stimulus inducing CRP production, in the liver by 35%. AGE decreased the level of interleukin‐1 receptor‐associated kinase 4 (IRAK4) by 60% and almost doubled the level of phospho‐AMP‐activated protein kinase (p‐AMPK) in the liver. Conclusion The anti‐atherosclerotic effect of AGE involves the suppression of inflammation by reducing the serum level of CRP and TXB 2 , and the protein level of TNF‐α and IRAK4, and increasing AMPK activity in liver.