BACKGROUND & AIMS: 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. CONCLUSION: Panaxatriol saponin ameliorated liver injury by APAP through restoring the expression TRX-1 and inhibiting pro-caspase-12 decrease.
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Wang et al. (2013) studied this question.