Gallic Acid Attenuates Dimethylnitrosamine-Induced Liver Fibrosis by Alteration of Smad Phosphoisoform Signaling in Rats

Biomed Res Int. 2018 Dec 2:2018:1682743. doi: 10.1155/2018/1682743. eCollection 2018.

Abstract

Dimethylnitrosamine (DMN) is a potent hepatotoxin, carcinogen, and mutagen. In our previous study, a candidate gallic acid (GA) that widely exists in food and fruit was selected for its capability to alleviate DMN toxicity in vivo. We aimed to investigate the therapeutic potential of GA against DMN-induced liver fibrosis. During the first four weeks, DMN was administered to rats via intraperitoneal injection every other day, except the control group. GA or silymarin was given to rats by gavage once daily from the second to the sixth week. GA significantly reduced liver damage in serum parameters and improved the antioxidant capacity in liver and kidney tissues. Cytokines involved in liver fibrosis were measured at transcriptional and translational levels. These results indicate that GA exhibits robust antioxidant and antifibrosis effects and may be an effective candidate natural medicine for liver fibrosis treatment.

MeSH terms

  • Animals
  • Dimethylnitrosamine / toxicity*
  • Gallic Acid / pharmacology*
  • Liver Cirrhosis* / chemically induced
  • Liver Cirrhosis* / metabolism
  • Liver Cirrhosis* / pathology
  • Liver Cirrhosis* / prevention & control
  • Male
  • Phosphoproteins / metabolism*
  • Protein Isoforms / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / drug effects*
  • Smad Proteins / metabolism*

Substances

  • Phosphoproteins
  • Protein Isoforms
  • Smad Proteins
  • Gallic Acid
  • Dimethylnitrosamine