BGP-15 Protects Mitochondria in Acute, Acetaminophen Overdose Induced Liver Injury

Research output: Contribution to journalArticle


Acetaminophen (APAP) induced hepatotoxicity involves activation of c-Jun amino-terminal kinase (JNK), mitochondrial damage and ER stress. BGP-15, a hydroximic acid derivative, has been reported to have hepatoprotective effects in APAP overdose induced liver damage. Effect of BGP-15 was further investigated on mitochondria in APAP-overdose induced acute liver injury in mice. We found that BGP-15 efficiently preserved mitochondrial morphology, and it caused a marked decrease in the number of damaged mitochondria. Attenuation of mitochondrial damage by BGP-15 is supported by immunohistochemistry as the TOMM20 label and the co-localized autophagy markers detected in the livers of APAP-treated mice were markedly reduced upon BGP-15 administration. This effect, along with the observed prevention of JNK activation likely contribute to the mitochondrial protective action of BGP-15.

Original languageEnglish
Pages (from-to)1797-1803
Number of pages7
JournalPathology and Oncology Research
Issue number3
Publication statusPublished - Jul 1 2020


  • Acetaminophen
  • BGP-15
  • Jun-kinase
  • Liver injury
  • Mitochondrium
  • Reduced glutathione

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Oncology
  • Cancer Research

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