Gallic Acid Attenuates Dimethylnitrosamine-Induced Liver Fibrosis by Alteration of Smad Phosphoisoform Signaling in Rats.
Yu-Xin ChenZiping ZhouQigui MoGao ZhouYou-Wei WangPublished in: BioMed research international (2018)
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.
Keyphrases
- liver fibrosis
- pet ct
- oxidative stress
- high glucose
- diabetic rats
- gene expression
- epithelial mesenchymal transition
- physical activity
- anti inflammatory
- drug induced
- randomized controlled trial
- endothelial cells
- risk assessment
- transforming growth factor
- signaling pathway
- climate change
- combination therapy
- stress induced
- heat shock protein