Protective Effects of Amarogentin against Carbon Tetrachloride-Induced Liver Fibrosis in Mice

Autor: Hang Zhao, Fang Wang, Ya Zhang, Tian Zhang, Si-Wang Wang, Hua Li, Wei Cao
Rok vydání: 2017
Předmět:
Liver Cirrhosis
0301 basic medicine
mitogen-activated protein kinase
Pharmaceutical Science
Plant Roots
Antioxidants
Analytical Chemistry
Mice
chemistry.chemical_compound
0302 clinical medicine
Fibrosis
Malondialdehyde
Drug Discovery
Iridoids
Tissue Distribution
Gentiana
Glycosides
Carbon Tetrachloride
liver fibrosis
chemistry.chemical_classification
amarogentin
Glutathione peroxidase
carbon tetrachloride
α-smooth muscle actin
Hydroxyproline
Chemistry (miscellaneous)
Molecular Medicine
030211 gastroenterology & hepatology
Nucleotides
Cyclic

medicine.medical_specialty
Down-Regulation
Biology
Article
Cell Line
Superoxide dismutase
03 medical and health sciences
Albumins
Internal medicine
medicine
Animals
Humans
Physical and Theoretical Chemistry
Cyclic guanosine monophosphate
Swertia
Dose-Response Relationship
Drug

Plant Extracts
Organic Chemistry
Amarogentin
medicine.disease
Actins
Mice
Inbred C57BL

Oxidative Stress
030104 developmental biology
Endocrinology
chemistry
Carbon tetrachloride
biology.protein
Phytotherapy
Zdroj: Molecules; Volume 22; Issue 5; Pages: 754
Molecules : A Journal of Synthetic Chemistry and Natural Product Chemistry
ISSN: 1420-3049
Popis: Amarogentin, a secoiridoid glycoside that is mainly extracted from Swertia and Gentiana roots, has been suggested to exhibit many biological effects, including anti-oxidative, anti-tumour, and anti-diabetic activities. The present study was designed to evaluate the protective effects of amarogentin on carbon tetrachloride-induced liver fibrosis in vivo and the underlying mechanism. Fibrosis was induced by subcutaneous injections of 6 mL/kg of 20% carbon tetrachloride (dissolved in olive oil) twice per week for seven weeks. Mice were orally treated with 25, 50, and 100 mg/kg amarogentin and with colchicine as a positive control. Biochemical assays and histopathological investigations showed that amarogentin delayed the formation of liver fibrosis; decreased alanine aminotransferase, aspartate aminotransferase, malondialdehyde and hydroxyproline levels; and increased albumin, cyclic guanosine monophosphate, glutathione peroxidase, and superoxide dismutase levels. Moreover, amarogentin exhibited downregulation of α-smooth muscle actin and transforming growth factor-β1 levels in immunohistochemical and Western blot analyses. The levels of phosphorylated extracellular regulated protein kinases, c-Jun N-terminal kinase, and p38 were also significantly reduced in all amarogentin-treated groups in a dose-dependent manner. These findings demonstrated that amarogentin exerted significant hepatoprotective effects against carbon tetrachloride-induced liver fibrosis in mice and suggested that the effect of amarogentin against liver fibrosis may be by anti-oxidative properties and suppressing the mitogen-activated protein kinase signalling pathway.
Databáze: OpenAIRE