title: Panaxatriol saponin ameliorated liver injury by acetaminophen via restoring thioredoxin-1 and pro-caspase-12.
abstract: OBJECTIVE
  Acetaminophen (APAP) is widely used as an antipyretic agent which is safe at therapeutic doses. However, overdose of APAP induces fatal and non-fatal hepatic necroses. The chemical reactive metabolites of APAP initiate toxicity and inflammatory response within the liver and lead to acute liver failure. However, the mechanism underlying APAP-induced liver injury is unknown. Thioredoxin-1 (TRX-1) is an important redox regulator, which plays roles in resisting oxidative stress, regulating inflammation and inhibiting apoptosis. Panaxatriol saponin (PTS) is one of the biologically active fractions of Panax notoginseng which is a traditional Chinese medicine. The aim of this study was to investigate the mechanism on PTS protecting liver from APAP hepatotoxicity.
  
  
  METHODS
  Mice were divided into three groups, control group, APAP group and APAP combined with PTS group. Alanine aminotransferase (ALT) and tumour necrosis factor-alpha (TNF-α) were detected by ELISA. TRX-1 and pro-caspase-12 were examined by Western blotting.
  
  
  RESULTS
  Our results showed PTS inhibited the levels of ALT and TNF-α by APAP. Pretreatment with PTS ameliorated liver injury induced by APAP. The decrease in TRX-1 expression was restored by PTS, as well as decreased pro-caspase-12 expression was inhibited by PTS. These data suggest that PTS has roles in suppressing the hepatotoxicity by APAP.
  
  
  CONCLUSIONS
  Panaxatriol saponin ameliorated liver injury by APAP through restoring the expression TRX-1 and inhibiting pro-caspase-12 decrease.
authors.affiliation: Faculty of Environmental Science and Engineering, Kunming University of Science and Technology, Kunming, China; Department of Science and Education Section, the seventh People's Hospital of Hangzhou, Hangzhou, China.
authors.forename: Shengdong
authors.initials: S
authors.lastname: Wang
authors.forename: Xiao
authors.initials: X
authors.lastname: Wang
authors.forename: Fucheng
authors.initials: F
authors.lastname: Luo
authors.forename: Xiaodan
authors.initials: X
authors.lastname: Tang
authors.forename: Kui
authors.initials: K
authors.lastname: Li
authors.forename: Xiaomei
authors.initials: X
authors.lastname: Hu
authors.forename: Jie
authors.initials: J
authors.lastname: Bai
mesh_terms: D000082:Acetaminophen / Q000009:adverse effects*; D000410:Alanine Transaminase / Q000097:blood; D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D053454:Caspase 12 / Q000378:metabolism; D056486:Chemical and Drug Induced Liver Injury / Q000188:drug therapy*; D004797:Enzyme-Linked Immunosorbent Assay; D036145:Ginsenosides / Q000494:pharmacology* / Q000627:therapeutic use; D051379:Mice; D013879:Thioredoxins / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D036145:Ginsenosides; D014409:Tumor Necrosis Factor-alpha; C515559:Txn1 protein, mouse; D000082:Acetaminophen; D013879:Thioredoxins; C004563:panaxatriol; D000410:Alanine Transaminase; D053454:Caspase 12
keywords: APAP; PTS; pro-caspase-12; thioredoxin