Quercetin-loaded exosomes derived from human umbilical cord mesenchymal stem cells alleviate microglia-mediated neuroinflammation via an anti-inflammatory mechanism
| dc.contributor.author | Osman, Sajeda | |
| dc.contributor.author | Demirbolat, Gulen Melike | |
| dc.contributor.author | Isik, Sevim | |
| dc.date.accessioned | 2026-11-05T11:07:12Z | |
| dc.date.issued | 2026 | |
| dc.description.abstract | Neuroinflammation is central to the progression of neurodegenerative diseases (NDs), with microglia contributing through the release of pro-inflammatory and oxidative mediators. Although quercetin (Que) possesses potent anti-inflammatory and antioxidant properties, its clinical application is limited by poor solubility and bioavailability. Umbilical cord mesenchymal stem cells (UC-MSCs)-derived exosomes (Exo) offer a promising delivery system to enhance Que efficacy. This study investigated the anti-inflammatory effects of Que-loaded Exo (Que-Exo) using an in vitro neuroinflammation model. Exo were isolated from UC-MSC-conditioned media via ultracentrifugation and loaded with Que through sonication. Characterization of Exo and Que-Exo was performed using dynamic light scattering, zeta potential analysis, transmission electron microscopy, and western blotting. In vitro release and cellular uptake studies assessed Que-Exo release profiles and their internalization by HMC3 microglial cells. Neuroinflammation was induced in HMC3 cells using lipopolysaccharide (LPS). The effects of Que-Exo on pro-inflammatory cytokine and enzyme expression, nitric oxide (NO) production, and inflammatory signaling pathways were evaluated using flow cytometry, the Griess assay, and western blotting. In vitro release from Que-Exo demonstrated improved stability and controlled delivery, while fluorescence imaging confirmed efficient uptake of Que-Exo by HMC3 cells. Mechanistically, Que-Exo inhibited NF-kappa B nuclear translocation, a key regulator of pro-inflammatory mediator transcription. Que-Exo pretreatment significantly reduced TNF-alpha, IL-6, iNOS, and COX-2 expression and suppressed NO synthesis in LPS-stimulated cells. Overall, Que-Exo exhibited superior anti-inflammatory activity compared to Exo and free Que, highlighting the synergistic effect of exosomal delivery in enhancing Que bioavailability and therapeutic efficacy against neuroinflammation. | |
| dc.description.issue | 5 | |
| dc.description.pages | 3469-3482 | |
| dc.description.sponsorship | Open access funding provided by the Scientific and Technological Research Council of Turkiye (TUB & Idot;TAK). | |
| dc.description.volume | 34 | |
| dc.identifier.doi | 10.1007/s10787-026-02236-z | |
| dc.identifier.issn | 0925-4692 | |
| dc.identifier.issn | 1568-5608 | |
| dc.identifier.uri | https://doi.org/10.1007/s10787-026-02236-z | |
| dc.identifier.uri | https://openaccess.acibadem.edu.tr/handle/11443/11430 | |
| dc.identifier.wos | WOS:001745161000001 | |
| dc.language.iso | en | |
| dc.publisher | SPRINGER BASEL AG | |
| dc.relation.funding | Uskudar University(Uskudar University) | |
| dc.relation.funding | Uskudar University | |
| dc.relation.hasversion | 10.1007/s10787-026-02236-z | |
| dc.relation.ispartof | INFLAMMOPHARMACOLOGY | |
| dc.subject | Neuroinflammation | |
| dc.subject | Lipopolysaccharide | |
| dc.subject | Microglia | |
| dc.subject | Mesenchymal stem cells | |
| dc.subject | Exosomes | |
| dc.subject | Quercetin | |
| dc.subject | ENHANCE | |
| dc.subject | BRAIN | |
| dc.subject | Immunology | |
| dc.subject | Pharmacology & Pharmacy | |
| dc.subject | Toxicology | |
| dc.title | Quercetin-loaded exosomes derived from human umbilical cord mesenchymal stem cells alleviate microglia-mediated neuroinflammation via an anti-inflammatory mechanism | |
| dc.type | Article | |
| oaire.citation.edition | Science Citation Index Expanded (SCI-EXPANDED) | |
| oaire.citation.endPage | 3482 | |
| oaire.citation.issue | 5 | |
| oaire.citation.startPage | 3469 | |
| oaire.citation.volume | 34 | |
| person.identifier.orcid | 0009-0008-7840-2823 | |
| person.identifier.rid | B-2807-2017 |
