Lemon Balm and Its Constituent, Rosmarinic Acid, Alleviate Liver Damage in an Animal Model of Nonalcoholic Steatohepatitis

• Published in: Nutrients 2020-04, Vol.12 (4), p.1166
• Main Authors: Kim, Myungsuk, Yoo, GyHye, Randy, Ahmad, Son, Yang-Ju, Hong, Chi Rac, Kim, Sang Min, Nho, Chu Won
• Format: Article
• Language: English
• Subjects: Adenosine; Adenosine kinase; Adenosine monophosphate; AMP-activated protein kinase (AMPK); AMP-Activated Protein Kinases - genetics; AMP-Activated Protein Kinases - metabolism; Animal models; Animals; anti-inflammation; Antioxidants; Cells, Cultured; Choline; Cinnamates - isolation & purification; Cinnamates - pharmacology; Cinnamates - therapeutic use; Cirrhosis; Collagen; Constituents; Depsides - isolation & purification; Depsides - pharmacology; Depsides - therapeutic use; Diet; Disease Models, Animal; Fatty liver; FDA approval; Fibrosis; Gene expression; Gene Expression - drug effects; Hep G2 Cells; Humans; Immunoglobulins; Inflammation; Kinases; Laboratory animals; lemon balm extract (LBE); Lipid metabolism; Lipid Metabolism - drug effects; Lipids; Liver; Liver - metabolism; Liver cirrhosis; Liver diseases; Male; Melissa - chemistry; Methionine; Mice, Inbred Strains; Non-alcoholic Fatty Liver Disease - drug therapy; Non-alcoholic Fatty Liver Disease - genetics; Non-alcoholic Fatty Liver Disease - metabolism; nonalcoholic steatohepatitis (NASH); Nutrient deficiency; Oxidative stress; Oxidative Stress - drug effects; Palmitic acid; Pathogenesis; Phytotherapy; Protein kinase; Proteins; Rosmarinic Acid; rosmarinic acid (RA); Signs and symptoms; Steatosis
• ISSN: 2072-6643; 2072-6643
• DOI: 10.3390/nu12041166

Nonalcoholic fatty liver disease (NAFLD) ranges in severity from hepatic steatosis to cirrhosis. Lemon balm and its major constituent, rosmarinic acid (RA), effectively improve the liver injury and obesity; however, their therapeutic effects on nonalcoholic steatohepatitis (NASH) are unknown. In this study, we investigated the effects of RA and a lemon balm extract (LBE) on NAFLD and liver fibrosis and elucidated their mechanisms. Palmitic acid (PA)-exposed HepG2 cells and db/db mice fed a methionine- and choline-deficient (MCD) diet were utilized to exhibit symptoms of human NASH. LBE and RA treatments alleviated the oxidative stress by increasing antioxidant enzymes and modulated lipid metabolism-related gene expression by the activation of adenosine monophosphate-activated protein kinase (AMPK) in vitro and in vivo. LBE and RA treatments inhibited the expression of genes involved in hepatic fibrosis and inflammation in vitro and in vivo. Together, LBE and RA could improve liver damage by non-alcoholic lipid accumulation and may be promising medications to treat NASH.