n/a
Abstract Title:

The natural product fucoidan ameliorates hepatic ischemia-reperfusion injury in mice.

Abstract Source:

Biomed Pharmacother. 2017 Oct ;94:687-696. Epub 2017 Aug 7. PMID: 28797984

Abstract Author(s):

Jingjing Li, QingHui Zhang, Sainan Li, Weiqi Dai, Jiao Feng, Liwei Wu, Tong Liu, Kan Chen, Yujing Xia, Jie Lu, Yingqun Zhou, Xiaoming Fan, Chuanyong Guo

Article Affiliation:

Jingjing Li

Abstract:

Fucoidan is a sulfated polysaccharide based predominantly on l-fucose, and has several biologic functions. Reactive oxygen species-mediated apoptosis and autophagy and release of related inflammatory factors have important roles in hepatic ischemia-reperfusion injury (IR). Here, the effect of fucoidan on hepatic IR was investigated. Mice were randomized into sham, IR, and fucoidan (20, 40mg/kg for 14days) groups. Samples were collected to assess biochemical indicators, hepatocyte damage and levels of proteins related to signaling pathways at different time points. Fucoidan had no effect on normal liver tissue, but inhibited the increases in alanine aminotransferase, aspartate transaminase, inflammatory factors, and the hepatocyte damage caused by IR. Also, apoptosis and autophagy via the activated JAK2/STAT1 pathway were attenuated by fucoidan to protect against hepatic injury. In conclusion, fucoidan ameliorates hepatic IR injury in mice via JAK2/STAT1-mediated apoptosis and autophagy. Inhibition of this pathway may be associated with reduced release of related inflammatory cytokines, especially interferon-γ.

Study Type : Animal Study

Print Options


Key Research Topics

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2024 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.