BGP-15 Protects Mitochondria in Acute, Acetaminophen Overdose Induced Liver Injury.
Farkas SarnyaiTimea SzekerczésMiklós CsalaBalázs SümegiAndrás SzarkaZsuzsa SchaffJózsef MandlPublished in: Pathology oncology research : POR (2019)
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.
Keyphrases
- drug induced
- liver injury
- oxidative stress
- cell death
- diabetic rats
- induced apoptosis
- reactive oxygen species
- endoplasmic reticulum
- high glucose
- endoplasmic reticulum stress
- liver failure
- type diabetes
- skeletal muscle
- mass spectrometry
- hepatitis b virus
- adipose tissue
- acute respiratory distress syndrome
- high resolution
- aortic dissection