The cytotoxic concentration of rosmarinic acid increases MG132-induced cytotoxicity, proteasome inhibition, autophagy, cellular stresses, and apoptosis in HepG2 cells

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dc.contributor.authorOzgun, G. S.
dc.contributor.authorOzgun, E.
dc.date.accessioned2024-06-12T11:13:45Z
dc.date.available2024-06-12T11:13:45Z
dc.date.issued2020
dc.departmentTrakya Üniversitesien_US
dc.description.abstractRosmarinic acid (RA) is a natural polyphenolic compound derived from many common herbal plants. Although it is known that RA has many important biological activities, its effect on proteasome inhibitor-induced changes in cancer treatment or its effects on any experimental proteasome inhibition model is unknown. The aim of the study was to investigate the effect of RA on MG132-induced cytotoxicity, proteasome inhibition, autophagy, cellular stresses, and apoptosis in HepG2 cells. HepG2 cells were treated with 10, 100, and 1000 mu M RA in the presence of MG132 for 24 h; 10 and 100 mu M RA did not affect but 1000 mu M RA decreased cell viability in HepG2 cells. MG132 caused a significant decrease in cell viability and phosphorylation of mammalian target of rapamycin and a significant increase in levels of polyubiquitinated protein, microtubule-associated proteins 1A/1B light chain 3B-II (LC3B-II), heat shock protein 70 (HSP70), binding immunoglobulin protein (BiP), activating transcription factor 4 (ATF4), protein carbonyl, and cleaved poly(adenosine diphosphate-ribose) polymerase 1 (PARP1); 10 and 100 mu M RA did not significantly change these effects of MG132 in HepG2 cells; 1000 mu M RA caused a significant decrease in cell viability and a significant increase in polyubiquitinated protein, LC3B-II, HSP70, BiP, ATF4, protein carbonyl, and cleaved PARP1 levels in MG132-treated cells. Our study showed that only 1000 mu M RA increased MG132-induced cytotoxicity, proteasome inhibition, autophagy, cellular stresses, and apoptosis in HepG2 cells. According to our results, cytotoxic concentration of RA can potentiate the effects of MG132 in hepatocellular carcinoma treatment.en_US
dc.identifier.doi10.1177/0960327119896614
dc.identifier.endpage523en_US
dc.identifier.issn0960-3271
dc.identifier.issn1477-0903
dc.identifier.issue4en_US
dc.identifier.pmid31876192en_US
dc.identifier.scopus2-s2.0-85077239606en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage514en_US
dc.identifier.urihttps://doi.org/10.1177/0960327119896614
dc.identifier.urihttps://hdl.handle.net/20.500.14551/23673
dc.identifier.volume39en_US
dc.identifier.wosWOS:000507187100001en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherSage Publications Ltden_US
dc.relation.ispartofHuman & Experimental Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectRosmarinic Aciden_US
dc.subjectProteasome Inhibitoren_US
dc.subjectHepatocellular Carcinomaen_US
dc.subjectAutophagyen_US
dc.subjectOxidative Stressen_US
dc.subjectApoptosisen_US
dc.subjectSignaling Pathwayen_US
dc.subjectMg132en_US
dc.subjectDegradationen_US
dc.subjectActivationen_US
dc.subjectLineen_US
dc.subjectProoxidanten_US
dc.subjectExpressionen_US
dc.subjectToxicityen_US
dc.subjectCleavageen_US
dc.subjectSystemsen_US
dc.titleThe cytotoxic concentration of rosmarinic acid increases MG132-induced cytotoxicity, proteasome inhibition, autophagy, cellular stresses, and apoptosis in HepG2 cellsen_US
dc.typeArticleen_US

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