Multi-tissue lipotoxicity caused by high-fat diet feeding is attenuated by the supplementation of Korean red ginseng in mice

Molecular & Cellular Toxicology

article

Jang, Seon-A¹  Avolio, Alberto P.²  Gangoda, Sumudu V. S.²  Koo, Hyun Jung³  Kim, Myung Kyum⁴  Kang, Se Chan¹  Sohn, Eun-Hwa⁵  Namkoong, Seung⁵  Lee, Sung Ryul⁶  Lee, Jin Woo⁵  Park, Yuna⁴  So, Gyeongseop⁵  Kim, Sung Hyeok⁵  Kim, Mi-Ja⁵  Jang, Ki-Hyo⁵ 

[1] Department of Oriental Medicine Biotechnology, College of Life Sciences, Kyung Hee University;Department of Biomedical Sciences, Faculty of Medicine and Health Sciences, Macquarie University;Department of Medicinal and Industrial Crops, Korea National College of Agriculture and Fisheries;Department of Bio and Environmental Technology, College of Natural Science, Seoul Women’s University;College of Health Sciences, Kangwon National University;Department of Convergence Biomedical Science, Cardiovascular and Metabolic Disease Center, College of Medicine, Inje University

关键词: Cell adhesion molecules;    High-fat diet;    Inflammation;    Korean red ginseng;    Lipotoxicity;   

DOI  :  10.1007/s13273-019-00056-7

来源: Korean Society of Toxicogenomics and Toxicoproteomics

【 摘 要 】

Background Excessive intake of fat, one of the causes of obesity, is associated with 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) on high-fat diet (HFD)-induced lipotoxicity and inflammatory responses in the aorta, liver, and brain. Methods Male C57BL/6 mice were fed HFD with or without KRG for 12 weeks. The improvement effect in KRG on lipotoxicity and inflammatory potential was determined in the blood and the aorta, liver, and brain tissues. Results KRG significantly inhibited 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activity by > 20% in vitro. KRG supplementation suppressed HFD-associated body weight gain, lipid profile changes, and excessive fat deposition in the liver and increased leptin, insulin, and ALT levels in the blood. Inflammatory markers in the aorta, liver, and brain were also significantly reduced by KRG treatment. In microvascular endothelial cells, the 15% cyclic stretch-mediated upregulation of ICAM-1 and vascular cell adhesion protein-1 (VCAM-1) expression was significantly attenuated in the presence of KRG. Conclusion KRG supplementation attenuates HFD-mediated body weight gain, lipid profile changes, and multi-tissue inflammatory responses.

【 授权许可】

Unknown