Anti-inflammatory and antioxidative actions of tacrolimus (FK506) on human microglial HMC3 cell line

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dc.authorid0000-0003-2594-502X
dc.authorid0000-0002-7248-7933
dc.contributor.authorKocanci, Fatma Gonca
dc.contributor.authorGoksu, Azize Yasemin
dc.date.accessioned2026-01-24T12:29:03Z
dc.date.available2026-01-24T12:29:03Z
dc.date.issued2024
dc.departmentAlanya Alaaddin Keykubat Üniversitesi
dc.description.abstractMicroglial cells are indispensable for the normal development and functioning of neurons in the central nervous system, where they play a crucial role in maintaining brain homeostasis by surveilling the microenvironment for signs of injury or stress and responding accordingly. However, in neurodegenerative diseases, the density and phenotypes of microglial cells undergo changes, leading to chronic activation and inflammation. Shifting the focus from neurons to microglia in drug discovery for neurodegenerative diseases has become an important therapeutic target. This study was aimed to investigate the potential of Tacrolimus (FK506) an FDA-approved calcineurin inhibitor, to modulate the pathology of neurodegenerative diseases through anti-inflammatory and antioxidative effects on microglial activation. The human microglia clone 3 (HMC3) cells were exposed to 1 mu g/mL LPS in the presence and absence of doses of FK506. Survival rates of cells were determined using the 3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide (MTT) method. Morphological evaluation of cells showed that FK506 restored the normal morphology of activated microglia. Furthermore, FK506 treatment increases the total antioxidant capacity and reduces the total oxidative capacity, indicating its potential antioxidant effects. Data from ELISA and RT-PCR analyses showed that LPS abolished its promoting effects on the release of proinflammatory IL-1 beta and IL-6 cytokines in HMC3 cells, reflecting the anti-inflammatory effect of FK506. These findings support the idea that FK506 could be a promising therapeutic agent for neurodegenerative diseases by modulating microglial activation and reducing inflammation and oxidative stress.
dc.description.sponsorshipThis study was supported by the Scientific Research Council of Akdeniz University (Grant number AU, TKA-2018-3933). [TKA-2018-3933]; Scientific Research Council of Akdeniz University
dc.description.sponsorshipThis study was supported by the Scientific Research Council of Akdeniz University (Grant number AU, TKA-2018-3933).
dc.identifier.doi10.1111/sji.13339
dc.identifier.issn0300-9475
dc.identifier.issn1365-3083
dc.identifier.issue2
dc.identifier.pmid38441214
dc.identifier.scopus2-s2.0-85176960389
dc.identifier.scopusqualityQ2
dc.identifier.urihttps://doi.org/10.1111/sji.13339
dc.identifier.urihttps://hdl.handle.net/20.500.12868/5100
dc.identifier.volume99
dc.identifier.wosWOS:001103829500001
dc.identifier.wosqualityQ2
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.language.isoen
dc.publisherWiley
dc.relation.ispartofScandinavian Journal of Immunology
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.snmzKA_WoS_20260121
dc.subjectcalcineurin inhibitor
dc.subjectin vitro
dc.subjectinflammation
dc.subjectmicroglia
dc.subjectoxidative stress
dc.subjecttacrolimus
dc.titleAnti-inflammatory and antioxidative actions of tacrolimus (FK506) on human microglial HMC3 cell line
dc.typeArticle

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