Hepatoprotective Effect of Ugonin M, A Helminthostachys zeylanica Constituent, on Acetaminophen-Induced Acute Liver Injury in Mice

• Published in: Molecules (Basel, Switzerland) Vol. 23; no. 10; p. 2420
• Main Authors: Wu, Kun-Chang, Ho, Yu-Ling, Kuo, Yueh-Hsiung, Huang, Shyh-Shyun, Huang, Guan-Jhong, Chang, Yuan-Shiun
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI 21.09.2018; MDPI AG
• Subjects: acetaminophen; Acetaminophen - adverse effects; acute liver injury; Acute Lung Injury - chemically induced; Acute Lung Injury - drug therapy; Acute Lung Injury - metabolism; Animals; anti-inflammatory; Anti-Inflammatory Agents - administration & dosage; Anti-Inflammatory Agents - chemistry; Anti-Inflammatory Agents - pharmacology; Antioxidants - administration & dosage; Antioxidants - chemistry; Antioxidants - pharmacology; Biomarkers - metabolism; Disease Models, Animal; Ferns - chemistry; Flavonoids - administration & dosage; Flavonoids - chemistry; Flavonoids - pharmacology; Gene Expression Regulation - drug effects; Helminthostachys zeylanica; hepatoprotective; Lipid Metabolism - drug effects; Lipid Peroxidation - drug effects; Liver - drug effects; Liver - metabolism; Male; Mice; Nitric Oxide - metabolism; Plant Extracts - administration & dosage; Plant Extracts - chemistry; Plant Extracts - therapeutic use; Ugonin M; anti-inflammatory; acetaminophen; Ugonin M; hepatoprotective; Helminthostachys zeylanica; acute liver injury
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules23102420

The present study aimed to discover the possible effectiveness of Ugonin M, a unique flavonoid isolated from -a traditional Chinese medicine used as anti-inflammatory medicine-and to elucidate the potential mechanisms of Ugonin M in the acute liver injury induced by acetaminophen (APAP). In this study, Ugonin M significantly ameliorated APAP-induced histopathological changes and the typical liver function biomarkers (i.e., alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (T-Bil)). It also affected APAP-induced abnormal lipid metabolism including total cholesterol (TC) and triglyceride (TG) in the serum. In inflammatory pharmacological action, Ugonin M suppressed the pro-inflammatory mediators such as nitric oxide (NO) and the lipid peroxidation indicator malondialdehyde (MDA). In addition, Ugonin M reinforced hemeoxygenase-1 (HO-1) protein expression and the production of antioxidant enzymes viz superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT). Furthermore, inflammation-associated cytokines including tumor necrosis factor- (TNF- ), interleukin-6 (IL-6), and IL-1 as well as proteins such as inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were decreased by the pretreatment of Ugonin M. Moreover, this study found that pretreatment of Ugonin M apparently decreased nuclear factor-kappa B (NF- B) and mitogen-activated protein kinases (MAPKs) activation via inhibition of the degradation of NF- B, inhibitory κB- (I B- ) extracellular regulated kinase (ERK), c-Jun- -terminal (JNK), and p38 active phosphorylation. In conclusion, Ugonin M significantly showed a protective effect against APAP-induced liver injury by reducing oxidative stress and inflammation. Thus, Ugonin M could be one of the effective components of that plays a major role in the treatment of inflammatory disorders.