Protective effects of geniposide against Tripterygium glycosides (TG)-induced liver injury and its mechanisms

J Toxicol Sci. 2016 Feb;41(1):165-73. doi: 10.2131/jts.41.165.


Tripterygium glycosides (TG) are commonly used for basic medicine in curing rheumatoid arthritis but with a high incidence of liver injury. Geniposide (GP) has broad and diverse bioactivities, but until now it is still unknown whether GP can protect against TG-induced liver injury. This study, for the first time, observed the possible protection of GP against TG-induced liver injury in mice and its mechanisms underlying. Oral administration of TG (270 mg/kg) induced significant elevation in the levels of serum alanine / aspartate transaminase (ALT/AST), hepatic malondialdehyde (MDA) and pro-inflammatory cytokine tumor necrosis factor-alpha (TNF-α) (all P < 0.01). On the other hand, remarkably decreased biomarkers, including hepatic glutathione (GSH) level, activities of glutathione transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD) and catalase (CAT), and anti-inflammatory cytokine interleukin (IL)-10, were observed following TG exposure (all P < 0.01). Nevertheless, all of these phenotypes were evidently reversed by pre-administration of GP for 7 continuous days. Further analysis showed that the mRNA expression of hepatic growth factor-beta1 (TGF-β1), one of tissue repair and regeneration cytokines, was enhanced by GP. Taken together, the current research suggests that GP protects against TG-induced liver injury in mice probably involved during attenuating oxidative stress and inflammation, and promoting tissue repair and regeneration.

Publication types

  • Letter
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Alanine Transaminase / metabolism
  • Animals
  • Anti-Inflammatory Agents
  • Antirheumatic Agents / administration & dosage*
  • Antirheumatic Agents / adverse effects
  • Chemical and Drug Induced Liver Injury / drug therapy*
  • Chemical and Drug Induced Liver Injury / prevention & control*
  • Gene Expression / drug effects
  • Glutathione / metabolism
  • Glycosides / administration & dosage*
  • Glycosides / adverse effects
  • Iridoids / administration & dosage*
  • Iridoids / pharmacology*
  • Liver / metabolism
  • Liver Regeneration / genetics
  • Male
  • Mice, Inbred Strains
  • Oxidative Stress / drug effects
  • Phytotherapy
  • RNA, Messenger / metabolism
  • Transforming Growth Factor beta1 / genetics
  • Transforming Growth Factor beta1 / metabolism
  • Tripterygium / chemistry*
  • Tumor Necrosis Factor-alpha / metabolism


  • Anti-Inflammatory Agents
  • Antirheumatic Agents
  • Glycosides
  • Iridoids
  • RNA, Messenger
  • Transforming Growth Factor beta1
  • Tumor Necrosis Factor-alpha
  • geniposide
  • Alanine Transaminase
  • Glutathione