Adenosine-rich extract of Ganoderma lucidum: A safe and effective lipid-lowering substance
He Li,
Yawei Du,
Hanrui Ji,
Yanan Yang,
Changchang Xu,
Qiaodan Li,
Longkai Ran,
Chongming Wu,
Qile Zhou,
Shengxian Wu
Affiliations
He Li
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China; Shandong University of Traditional Chinese Medicine, Shandong 250355, China
Yawei Du
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
Hanrui Ji
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
Yanan Yang
Pharmacology and Toxicology Research Center, Institute of Medicinal Plant Development, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100193, China
Changchang Xu
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
Qiaodan Li
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
Longkai Ran
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China
Chongming Wu
School of Chinese Materia Medica, Tianjin University of Traditional Chinese Medicine, Tianjin 301617, China; Corresponding author
Qile Zhou
Beijing Institute of Nutritional Resources, Beijing Academy of Science and Technology, Beijing 100069, China; Corresponding author
Shengxian Wu
Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing 100700, China; Corresponding author
Summary: Ganoderma lucidum is a traditional Chinese medicine with a variety of active compounds and possesses adequate lipid-lowering and anti-atherosclerotic effects. However, its main active components and potential mechanisms still remain unclear. Here, we evaluated the anti-hyperlipidemic effect of the adenosine extract from Ganoderma lucidum (AEGL) in high-fat-diet (HFD)-induced hyperlipidemic ApoE−/− mice and explored the underlying biological mechanism by multi-omics analysis. Treatment with AEGL for 8 weeks significantly decreased the serum levels of total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-c) by 45.59%, 41.22%, and 39.02%, respectively, as well as reduced liver TC and TG by 44.15% and 76.23%, compared with the HFD-only group. We also observed significant amelioration of hepatic steatosis without liver and kidney damage after AEGL treatment. Regulating the expression and acetylation/crotonylation of proteins involved in the PPAR signaling pathway may be one of the potential mechanisms involved in the observed lipid-lowering effects of AEGL.
