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

Sarnyai, Szekerczés, Csala, Sümegi, Szarka, Schaff, Mandl (2020) BGP-15 Protects Mitochondria in Acute, Acetaminophen Overdose Induced Liver Injury Pathol Oncol Res (IF: 2.8) 26(3) 1797-1803

Abstract

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.

Links

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7297855
http://www.ncbi.nlm.nih.gov/pubmed/31705481
http://dx.doi.org/10.1007/s12253-019-00721-1

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