Mitigating Effect of Korea Red Ginseng Against Multi‐Tissue Iipotoxicity Caused by High‐Fat Diet Feeding

Abstract

BackgroundsExcessive consumption of fat and its aberrant deposit in the body has been linked to the low‐grade inflammation in various susceptible organs and eventually causes tissue toxicity. This study examines the multifaceted suppressive effects of Korean Red ginseng extract (KRG) against high‐fat diet (HFD)‐induced lipotoxicity and inflammatory responses occurring in the liver, aorta, and brain.MethodsThe standardized KRG powder was prepared by Korea Ginseng Corporation and was dissolved in phosphate buffered saline as a concentration of 30 mg/mL. Male C57BL/6 mice were fed HFD with or without KRG (10 or 50 mg/kg body weight; orally) for 12 weeks (n = 10 per group). The anti‐inflammatory potential of KRG was determined in the blood and the aorta, liver, and brain.ResultsKRG significantly inhibited HMG‐CoA reductase activity in vitro. In vivo, KRG supplementation suppressed HFD‐associated body weight gain, lipid profile changes, excessive fat deposition in the liver, and increases of leptin, insulin, and ALT levels in the blood. Inflammatory markers of the aorta (ICAM‐1 protein level and wall thickening of the aorta), liver (COX‐2 expression and liver function tests), and brain (APP, BACE1, and Tau protein levels) were also significantly reduced by KRG. In microvascular endothelial cells, 15% cyclic stretch‐mediated upregulation of ICAM‐1 and VCAM‐1 expression was significantly attenuated in the presence of KRG.ConclusionKRG supplementation attenuates HFD‐mediated body weight gain, lipid profile changes, and multi‐tissue inflammatory responses including the liver, aorta, and brain.