Investigating the Effects of Curcumin on Lipid Metabolism and Cell Viability in HepG2 Cells: Potential Therapeutic Implications for Nonalcoholic Fatty Liver Disease

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dc.contributor.authorQaleban, Faeze
dc.contributor.authorMohammadnejad, Javad
dc.contributor.authorDaemi, Amin
dc.contributor.authorOzbolat, Guluzar
dc.contributor.authorDogus, Yusuf
dc.date.accessioned2026-04-25T14:19:44Z
dc.date.available2026-04-25T14:19:44Z
dc.date.issued2025
dc.departmentSinop Üniversitesi
dc.description.abstractMetabolic dysfunction-associated steatotic liver disease (MASLD), poses a significant global health challenge, necessitating novel therapeutic strategies. This study investigates examines the efficacy of curcumin (Cur), a natural bioactive compound, in suppressing inhibiting the proliferation of hepatocellular carcinoma proliferation and reducing lipid accumulation in vitro. HepG2 cells were treated with Cur (1.25-10 mu g/mL) for 24-72 h, revealing a dose- and time-dependent reduction in viability, with an IC50 of 10 mu g/mL at 72 h. Oil Red O staining demonstrated Cur's lipid-lowering effects, reducing lipid content by 57% at 5 mu g/mL and 78% at 10 mu g/mL, suggesting enhanced efficacy at higher concentrations. Quantitative Reverse Transcription Polymerase Chain Reaction (qRT-PCR) analysis revealed that Cur downregulated key lipogenic regulators Peroxisome proliferator-activated receptor gamma (PPAR gamma) and CCAAT/enhancer-binding protein alpha (C/EBP-alpha) by 2.3- and 1.8-fold, respectively, while modulating 14-3-3 gamma/beta expression, implicating these pathways in its mechanism. These findings highlight Cur's potential to attenuate hepatic lipid accumulation and cancer cell growth in vitro, warranting further validation in primary hepatocytes and preclinical models to advance its therapeutic prospects for Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD).
dc.description.sponsorshipThe authors received no specific funding for this work.
dc.description.sponsorshipThe authors have nothing to report.
dc.identifier.doi10.1002/ddr.70142
dc.identifier.issn0272-4391
dc.identifier.issn1098-2299
dc.identifier.issue5
dc.identifier.orcid0000-0002-0918-0621
dc.identifier.pmid40778534
dc.identifier.scopus2-s2.0-105012852846
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1002/ddr.70142
dc.identifier.urihttps://hdl.handle.net/11486/8129
dc.identifier.volume86
dc.identifier.wosWOS:001546255100001
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofDrug Development Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WOS_20260420
dc.subjectCell viability
dc.subjectCurcumin
dc.subjectDrug
dc.subjectLipid accumulation
dc.subjectNonalcoholic Fatty Liver Disease
dc.subjectPPAR signaling pathway
dc.titleInvestigating the Effects of Curcumin on Lipid Metabolism and Cell Viability in HepG2 Cells: Potential Therapeutic Implications for Nonalcoholic Fatty Liver Disease
dc.typeArticle

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