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Molecules. 2017 May 6;22(5). pii: E754. doi: 10.3390/molecules22050754.

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

Author information

1
Department of Natural Medicine, School of Pharmacy, Fourth Military University, 169 West Changle Road, Xi'an 710032, China. lmlx2428@163.com.
2
Department of Natural Medicine, School of Pharmacy, Fourth Military University, 169 West Changle Road, Xi'an 710032, China. zhaohang169@163.com.
3
Department of Natural Medicine, School of Pharmacy, Fourth Military University, 169 West Changle Road, Xi'an 710032, China. lihuasmile@aliyun.com.
4
Department of Natural Medicine, School of Pharmacy, Fourth Military University, 169 West Changle Road, Xi'an 710032, China. caowei@fmmu.edu.cn.
5
Department of Natural Medicine, School of Pharmacy, Fourth Military University, 169 West Changle Road, Xi'an 710032, China. wangfang3463704@163.com.
6
Xi'an Day Natural Inc., F501 Gazelle Valley, Pioneering R&D Park, 69 Jinye Road, Xi'an 710077, China. tian@daynatural.com.
7
Department of Natural Medicine, School of Pharmacy, Fourth Military University, 169 West Changle Road, Xi'an 710032, China. wangsiw@fmmu.edu.cn.

Abstract

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.

KEYWORDS:

amarogentin; carbon tetrachloride; liver fibrosis; mitogen-activated protein kinase; α-smooth muscle actin

PMID:
28481234
PMCID:
PMC6154739
DOI:
10.3390/molecules22050754
[Indexed for MEDLINE]
Free PMC Article

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