Phyllanthin inhibits CCl4-mediated oxidative stress and hepatic fibrosis by down-regulating TNF-α/NF-κB, and pro-fibrotic factor TGF-β1 mediating inflammatory signaling.

Abstract

Hepatic fibrosis is an important outcome of chronic liver injury and results in excess synthesis and accumulation of extracellular matrix (ECM) components. Phyllanthin (PLN) isolated from Phyllanthus amarus exhibits strong antioxidative property and protects HepG2 cells from carbon tetrachloride (CCl4)-induced experimental toxicity. The present study reports the antifibrotic potential of PLN. The in vivo inhibitory effect of PLN on CCl4-mediated lipid peroxidation and important profibrotic mediator transforming growth factor β1 and on predominant ECM components collagen and fibronectin were also studied. The results show that PLN acts by suppressing the expression of inflammatory cytokine tumor necrosis factor-α and prevents activation of nuclear factor-κB in hepatic tissue. Our study highlights the molecular mechanism responsible for the antifibrotic efficacy of PLN.

• Authors: Rajesh Krithika, Vasavan Jyothilakshmi, Ramtej Jayaram Verma
• Journal: Toxicology and industrial health (Toxicol Ind Health) Vol. 32 Issue 5 Pg. 953-60 (May 2016) ISSN: 1477-0393 [Electronic] England
• PMID: 24817434 (Publication Type: Journal Article)
• Copyright: © The Author(s) 2014.

Chemical References

• Antioxidants
• Lignans
• NF-kappa B
• Plant Extracts
• Protective Agents
• RNA, Messenger
• Transforming Growth Factor beta1
• Tumor Necrosis Factor-alpha
• phyllanthin
• Carbon Tetrachloride

Topics

• Animals
• Antioxidants (pharmacology)
• Carbon Tetrachloride (toxicity)
• Chemical and Drug Induced Liver Injury (drug therapy)
• Down-Regulation
• Female
• Hep G2 Cells
• Humans
• Lignans (pharmacology)
• Lipid Peroxidation (drug effects)
• Liver (cytology, drug effects, metabolism)
• Liver Cirrhosis (chemically induced, drug therapy)
• Mice
• NF-kappa B (genetics, metabolism)
• Oxidative Stress (drug effects)
• Phyllanthus (chemistry)
• Plant Extracts (pharmacology)
• Protective Agents (pharmacology)
• RNA, Messenger (genetics, metabolism)
• Signal Transduction
• Transforming Growth Factor beta1 (genetics, metabolism)
• Tumor Necrosis Factor-alpha (genetics, metabolism)