title: Protective effects of geniposide against Tripterygium glycosides (TG)-induced liver injury and its mechanisms.
abstract: 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.
authors.affiliation: Collaborative Innovation Center for Respiratory Disease Diagnosis and Treatment & Chinese Medicine Development of Henan Province, Henan University of Traditional Chinese Medicine, China.
authors.forename: Junming
authors.initials: J
authors.lastname: Wang
authors.forename: Mingsan
authors.initials: M
authors.lastname: Miao
authors.forename: Lingbo
authors.initials: L
authors.lastname: Qu
authors.forename: Ying
authors.initials: Y
authors.lastname: Cui
authors.forename: Yueyue
authors.initials: Y
authors.lastname: Zhang
mesh_terms: D000284:Administration, Oral; D000410:Alanine Transaminase / Q000378:metabolism; D000818:Animals; D000893:Anti-Inflammatory Agents; D018501:Antirheumatic Agents / Q000008:administration & dosage* / Q000009:adverse effects; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy* / Q000517:prevention & control*; D015870:Gene Expression / Q000187:drug effects; D005978:Glutathione / Q000378:metabolism; D006027:Glycosides / Q000008:administration & dosage* / Q000009:adverse effects; D039823:Iridoids / Q000008:administration & dosage* / Q000494:pharmacology*; D008099:Liver / Q000378:metabolism; D008115:Liver Regeneration / Q000235:genetics; D008297:Male; D008815:Mice, Inbred Strains; D018384:Oxidative Stress / Q000187:drug effects; D008517:Phytotherapy; D012333:RNA, Messenger / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism; D029757:Tripterygium / Q000737:chemistry*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D018501:Antirheumatic Agents; D006027:Glycosides; D039823:Iridoids; D012333:RNA, Messenger; D053773:Transforming Growth Factor beta1; D014409:Tumor Necrosis Factor-alpha; C007835:geniposide; D000410:Alanine Transaminase; D005978:Glutathione