Boric Acid Reverses Nicotine-Induced Cytokine Expressions of Human Gingival Fibroblasts

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dc.authoridHakki, Sema/0000-0001-8665-6235
dc.authoridBozkurt, Serife Buket/0000-0002-8641-2844
dc.contributor.authorBozkurt, Serife Buket
dc.contributor.authorNielsen, Forrest H.
dc.contributor.authorHakki, Sema S.
dc.date.accessioned2024-11-07T13:34:33Z
dc.date.available2024-11-07T13:34:33Z
dc.date.issued2023
dc.departmentNiğde Ömer Halisdemir Üniversitesi
dc.description.abstractNicotine, the major bioactive ingredient in tobacco, is a major risk factor for periodontal disease and destruction. Nicotine has been shown to stimulate the production of cytokines that are priming agents for inflammation that induces tissue destruction, such as IL-1 beta, IL-6, and IL-8, by gingival keratinocytes and human gingival fibroblasts (HGF). Boron as boric acid has been found to decrease pro-inflammatory cytokines and increase anti-inflammatory cytokines in cells with inflammatory stress. Thus, a study was performed to determine whether boric acid reverses negative effects of nicotine on human gingival fibroblasts (HGFs). The viability and cytokine expressions of HGFs cultured for 24 and 72 h in control medium with no nicotine or boric acid added and in media containing only nicotine, only boric acid, or a combination of BA and nicotine were determined. Nicotine in concentrations of 10(-1), 10(-2), 10(-3),10(-4), 10(-5), and 10(-6) mM significantly reduced cell viability compared to the control. Boric acid at 10 and 50 ng/mL in the media partially restored and 100 ng/mL in the media fully restored the nicotine-depressed HGF cell viability to the same level as the control group. Nicotine elevated the expression of pro-inflammatory cytokines TNF-alpha, IL-1 beta, IL-6, IL-8, and IL-17 and decreased the anti-inflammatory IL-10 in HGFs at 24 and 72 h. Boric acid at 100 ng/mL in the medium prevented the changes induced by nicotine alone. The findings indicate that boric acid can inhibit or reverse nicotine-induced pathology in periodontal tissue and thus may help maintain oral and periodontal health in tobacco users.
dc.identifier.doi10.1007/s12011-022-03243-1
dc.identifier.endpage1180
dc.identifier.issn0163-4984
dc.identifier.issn1559-0720
dc.identifier.issue3
dc.identifier.pmid35441257
dc.identifier.scopus2-s2.0-85128420382
dc.identifier.scopusqualityQ1
dc.identifier.startpage1174
dc.identifier.urihttps://doi.org/10.1007/s12011-022-03243-1
dc.identifier.urihttps://hdl.handle.net/11480/16045
dc.identifier.volume201
dc.identifier.wosWOS:000784274400001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherSpringernature
dc.relation.ispartofBiological Trace Element Research
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_20241106
dc.subjectBoric acid
dc.subjectNicotine
dc.subjectCytokine
dc.subjectHuman gingival fibroblast
dc.titleBoric Acid Reverses Nicotine-Induced Cytokine Expressions of Human Gingival Fibroblasts
dc.typeArticle

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