Angelica sinensis polysaccharide attenuates concanavalin A-induced liver injury in mice

Int Immunopharmacol. 2016 Feb:31:140-8. doi: 10.1016/j.intimp.2015.12.021. Epub 2015 Dec 30.

Abstract

Angelica sinensis polysaccharide (ASP), extracted from the roots of A. sinensis (Oliv.) Diels, is a β-D-pyranoid polysaccharide with an average molecular weight of 72,900 Da. In this study, we investigated the protective effects of ASP against concanavalin A-induced liver failure and the underlying mechanisms. Concentrations of ASP ranging from 5 to 125 μg/mL could inhibit concanavalin A (ConA)-induced lymphoproliferative response. The potential hepatoprotective activity of ASP was demonstrated by the significant decrease in serum transaminase (ALT and AST) levels and the attenuation of liver inflammation damage exhibited by H&E stain of the liver. Furthermore, ASP pretreatment significantly decreased proinflammatory cytokines (TNF-α, IFN-γ, IL-2 and IL-6) and alleviated oxidative stress by reducing MDA and ROS levels and by enhancing SOD activity after ConA administration in mice. Results of Western blot analysis indicated that ASP attenuated Caspase-3-dependent apoptosis by Caspase-8 and JNK-mediated pathway and inhibited the activation of IL-6/STAT3 and NF-κB signaling pathways in ConA-induced liver damage in mice. In conclusion, ASP pretreatment could attenuate concanavalin A-induced liver injury through its anti-inflammatory and anti-oxidant actions in mice.

Keywords: Angelica sinensis polysaccharide; Concanavalin A; JNK; NF-κB; Oxidative stress; Proinflammatory cytokine.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Angelica sinensis / immunology*
  • Animals
  • Antigens, Plant / administration & dosage*
  • Chemical and Drug Induced Liver Injury / drug therapy*
  • Concanavalin A
  • Cytokines / metabolism
  • Female
  • Humans
  • Liver / drug effects*
  • Liver / metabolism
  • Mice
  • NF-kappa B / metabolism
  • Plant Roots
  • Polysaccharides / administration & dosage*
  • STAT3 Transcription Factor / metabolism
  • Signal Transduction / drug effects

Substances

  • Antigens, Plant
  • Cytokines
  • NF-kappa B
  • Polysaccharides
  • STAT3 Transcription Factor
  • Stat3 protein, mouse
  • Concanavalin A