000170446 001__ 170446
000170446 005__ 20260420103355.0
000170446 0247_ $$2doi$$a10.1038/s41598-026-42357-7
000170446 0248_ $$2sideral$$a148931
000170446 037__ $$aART-2026-148931
000170446 041__ $$aeng
000170446 100__ $$aRemirez de Ganuza, Cristina$$uUniversidad de Zaragoza
000170446 245__ $$aExploring the anti-inflammatory effects of genistein in an in vitro lipopolysaccharide-induced macrophage model
000170446 260__ $$c2026
000170446 5060_ $$aAccess copy available to the general public$$fUnrestricted
000170446 5203_ $$aInflammation plays a central role in the onset and progression of numerous diseases, and macrophages are key regulators of this process through their polarization toward pro- or anti-inflammatory phenotypes. Natural bioactive compounds have emerged as promising candidates to modulate inflammatory responses. Amongst these, genistein, a soybean-derived isoflavone, was selected due to its reported anti-inflammatory and antioxidant profile across different cell types. In this study, we evaluated the effects of genistein in a lipopolysaccharide (LPS)-induced macrophage model to investigate its cellular and molecular mechanisms of action. Genistein treatment at subcytotoxic concentration preserved cell viability, did not induce apoptosis or cell cycle arrest, and reduced oxidative stress. In LPS-stimulated macrophages, treatment with 5 µg/mL genistein significantly decreased nitric oxide production and downregulated pro-inflammatory markers while upregulating an anti-inflammatory mediator, thus reverting macrophage polarization to an anti-inflammatory phenotype. Protein analyses confirmed reduced expression of iNOS and cytokines such as IL-6 and TNF-α. Furthermore, genistein restored cell morphology and inhibited NF-κB p65 nuclear translocation, indicating its capacity to counteract LPS-driven pro-inflammatory signalling. These findings support the role of genistein in modulating macrophage polarization and inflammatory responses, highlighting its therapeutic potential for the management of acute and chronic inflammation-related disorders.
000170446 536__ $$9info:eu-repo/grantAgreement/ES/DGA/B55_24$$9info:eu-repo/grantAgreement/ES/IISAragón/FSE-I-01/Intramural23$$9info:eu-repo/grantAgreement/ES/ISCIII/FIS/PI21-00911$$9info:eu-repo/grantAgreement/ES/ISCIII/FORT23-00028
000170446 540__ $$9info:eu-repo/semantics/openAccess$$aby-nc-nd$$uhttps://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
000170446 655_4 $$ainfo:eu-repo/semantics/article$$vinfo:eu-repo/semantics/publishedVersion
000170446 700__ $$aLópez, Sonia
000170446 700__ $$0(orcid)0000-0003-2293-363X$$aMendoza, Gracia
000170446 7102_ $$15005$$2555$$aUniversidad de Zaragoza$$bDpto. Ing.Quím.Tecnol.Med.Amb.$$cÁrea Ingeniería Química
000170446 773__ $$g16, 1 (2026), [12 pp.]$$pSci. rep. (Nat. Publ. Group)$$tScientific reports (Nature Publishing Group)$$x2045-2322
000170446 8564_ $$s2552447$$uhttps://zaguan.unizar.es/record/170446/files/texto_completo.pdf$$yVersión publicada
000170446 8564_ $$s2481654$$uhttps://zaguan.unizar.es/record/170446/files/texto_completo.jpg?subformat=icon$$xicon$$yVersión publicada
000170446 909CO $$ooai:zaguan.unizar.es:170446$$particulos$$pdriver
000170446 951__ $$a2026-04-18-10:49:43
000170446 980__ $$aARTICLE