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

dc.contributor.author	Sarnyai, Farkas
dc.contributor.author	Szekerczés, Tímea
dc.contributor.author	Csala, Miklós
dc.contributor.author	Sümegi, Balázs
dc.contributor.author	Szarka, András
dc.contributor.author	Schaff, Zsuzsa
dc.contributor.author	Mandl, József
dc.date.accessioned	2021-09-03T07:27:12Z
dc.date.available	2021-09-03T07:27:12Z
dc.date.issued	2019
dc.identifier.citation	journalVolume=26;journalIssueNumber=3;journalTitle=PATHOLOGY AND ONCOLOGY RESEARCH;pagerange=1797-1803;journalAbbreviatedTitle=PATHOL ONCOL RES;
dc.identifier.uri	http://repo.lib.semmelweis.hu//handle/123456789/8003
dc.identifier.uri	doi:10.1007/s12253-019-00721-1
dc.description.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.
dc.format.extent	1797-1803
dc.relation.ispartof	urn:issn:1219-4956
dc.title	BGP-15 Protects Mitochondria in Acute, Acetaminophen Overdose Induced Liver Injury
dc.type	Journal Article
dc.date.updated	2019-11-25T12:48:18Z
dc.language.rfc3066	en
dc.rights.holder	NULL
dc.identifier.mtmt	30900106
dc.identifier.wos	000495186100001
dc.identifier.pubmed	31705481
dc.contributor.department	SE/AOK/I/Orvosi Vegytani, Molekuláris Biológiai és Patobiokémiai Intézet
dc.contributor.department	SE/AOK/I/II. Sz. Patológiai Intézet
dc.contributor.institution	Semmelweis Egyetem
dc.mtmt.swordnote	Megosztott első szerzőség!