Literature DB >> 25201143

Danshensu-mediated protective effect against hepatic fibrosis induced by carbon tetrachloride in rats.

W Qu1, H Huang2, K Li3, C Qin4.   

Abstract

The culprit of hepatic fibrosis (HF) is linked to suprathreshold deposition of collagen. Thus, collagen reduction by improved metabolism contributes to HF management. In this study, we aimed to investigate the hepatoprotective effects of Danshensu (DSS) against carbon tetrachloride (CCl4)-induced HF rats. The results showed that DSS-administrated rats resulted in decreasing in hepatosomatic indexes, and lowering serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Meanwhile, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were increased, while the content of malonaldehyde (MDA) was lessened in liver tissue of DSS administration group. In addition, the pro-fibrotic markers of hydroxyproline (Hyp), type III procollagen (PCIII) and hyaluronic acid (HA) contents were decreased. Histopathological examination confirmed that the hepatotoxicity in CCl4-injured rats was alleviated following the DSS administration. Furthermore, intrahepatic protein expressions of alpha-smooth muscle actin (α-SMA), phosphorylated JAK2 (p-JAK2) and phosphorylated STAT3 (p-STAT3) were effectively down-regulated, respectively. Overall, this work demonstrates that DSS played the protective effect against CCl4-induced cytotoxicity in liver tissue, which the probable mechanism is associated with attenuation of lipid peroxidation, collagen accumulation and enhancement of anti-oxidative defense capability, as well as regulation of intrahepatic JAK/STAT pathway for maintaining collagenic homoeostasis.
Copyright © 2014 Elsevier Masson SAS. All rights reserved.

Entities:  

Keywords:  Carbon tetrachloride; Danshensu; Fibrose hépatique; Hepatic fibrosis; Hepatoprotection; Hépatoprotection; Metabolism; Métabolisme

Mesh:

Substances:

Year:  2014        PMID: 25201143     DOI: 10.1016/j.patbio.2014.07.008

Source DB:  PubMed          Journal:  Pathol Biol (Paris)        ISSN: 0369-8114


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