Capsaicin inhibits cell proliferation by enhancing oxidative stress and apoptosis through SIRT1/NOX4 signaling pathways in HepG2 and HL-7702 cells

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dc.authoridHacıoğlu, Ceyhan/0000-0002-0993-6118
dc.contributor.authorHacıoğlu, Ceyhan
dc.date.accessioned2023-07-26T11:50:03Z
dc.date.available2023-07-26T11:50:03Z
dc.date.issued2022
dc.departmentDÜ, Tıp Fakültesi, Temel Tıp Bilimleri Bölümü, Tıbbi Biyokimya Ana Bilim Dalıen_US
dc.description.abstractCapsaicin could suppress the proliferation of cancer cells and inhibit many biochemical pathways associated with tumorigenesis and metastasis. This study investigates the effects of capsaicin in both hepatocellular carcinoma (HepG2) and normal hepatocytes (HL-7702) via the SIRT1/NOX4 signaling pathway. After determination of cytotoxic concentrations of capsaicin on HL-7702 and HepG2 cells, we measured total oxidant status (TOS), reduced glutathione (GSH), 8-hydroxydeoxyguanosine (8-OHdG), cytochrome c (CYC), caspase3 (CASP3), Bcl-2, Bax, sirtuin1 (SIRT1), and NADPH oxidases4 (NOX4) levels. Besides this, we analyzed the messenger RNA and protein levels of SIRT1 and NOX4. We found that capsaicin increased TOS, 8-OHdG, CASP3, CYC, Bax, and NOX4 levels, and decreased Bcl-2, GSH, and SIRT1 in a concentration-dependent manner in HepG2 cells. However, especially low capsaicin concentration (128.75 mu M) enhanced GSH and SIRT levels and reduced TOS, CASP3, CYC, 8-OHdG, and NOX4 levels in HL-7702 cells (p < 0.05). Interestingly, 128.75 and 172.8 mu M capsaicin treatment increased SIRT1 expression levels in HL-7702 cells, resulting in an increase in GSH levels and a decrease in TOS, CYC, CAPS3, and 8-OHdG levels through NOX4 inhibition. Furthermore, we demonstrated a significant decrease in SIRT1 protein levels and an increase in NOX4 protein levels and caspase-3/-7 activities in both HL-7702 and HepG2 cells treated with 261.5 mu M capsaicin. Additionally, morphological changes in HL-7702 and HepG2 cells treated with capsaicin correlated with the enhancement in oxidative burden, DNA damage, and apoptosis. Our results show that capsaicin effectively might cause higher oxidative, apoptotic, and DNA damage in HepG2 cells than in HL-7702 cells through the SIRT1/NOX4 signaling pathway.en_US
dc.identifier.doi10.1002/jbt.22974
dc.identifier.issn1095-6670
dc.identifier.issn1099-0461
dc.identifier.issue3en_US
dc.identifier.pmid34939720en_US
dc.identifier.scopus2-s2.0-85121598570en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.urihttps://doi.org/10.1002/jbt.22974
dc.identifier.urihttps://hdl.handle.net/20.500.12684/12216
dc.identifier.volume36en_US
dc.identifier.wosWOS:000733385000001en_US
dc.identifier.wosqualityQ2en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakPubMeden_US
dc.indekslendigikaynakScopusen_US
dc.institutionauthorHacıoğlu, Ceyhan
dc.language.isoenen_US
dc.publisherWileyen_US
dc.relation.ispartofJournal of Biochemical and Molecular Toxicologyen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.snmz$2023V1Guncelleme$en_US
dc.subjectApoptosis; Capsaicin; Dna Damage Sirt1; Hepg2; Hl-7702; Nox4; Oxidative Stressen_US
dc.subjectNadph Oxidases; Anticancer Properties; Cancer Cells; Nox Family; In-Vitro; Generation; Induction; Roles; Deathen_US
dc.titleCapsaicin inhibits cell proliferation by enhancing oxidative stress and apoptosis through SIRT1/NOX4 signaling pathways in HepG2 and HL-7702 cellsen_US
dc.typeArticleen_US

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