Browsing by Author "Cakir, Serife"

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Imiquimod-Induced Psoriasis-Like Inflammation Model in Calcium-Differentiated Human Keratinocytes Mimics Psoriasis-Associated Biomolecules and Signaling Pathways
(Springer Nature, 2025) Çakır, Mustafa; Keskin, S.; Uyanikgil, Yiǧit; Cakir, Serife; Açıkgöz, Eda
Dysregulation of keratinocytes and immune response are remarkable phenomena that trigger inflammation in the psoriasis pathology. In vitro models for elucidating psoriasis pathogenesis and treatment provide the potential to mimic enhanced systems that more accurately represent the disease phenotype and immunopathogenesis. The aim of this study was to investigate the morphological, molecular and biochemical changes of cell–cell interactions in CaCl₂-differentiated HaCaT cells under imiquimod (IMQ)-induced inflammatory conditions. To establish this model, HaCaT cells were differentiated with CaCl₂ and then stimulated with IMQ to induce psoriatic inflammation. Morphological analyses were evaluated on inverted microscope images and HE-stained cells under light microscopy. Cell proliferation was analyzed by the MTT assay and confirmed with the PCNA biomarker. Psoriasis-associated biomarkers were evaluated by immunofluorescence staining. Cytokine levels were measured by ELISA, and the expressions of Toll-like receptors (TLRs), NLRP3 inflammasome, angiogenic, hypoxia, and TGF-β/Smads genes were assessed by qRT-PCR. The results revealed that IMQ-induced HaCaT cells exhibited morphology and organization mimicking psoriatic keratinocytes. The expressions of CK17, PCNA, actin, prohibitin and inflammatory cytokines were significantly increased in the IMQ group. Furthermore, significant changes were detected in the gene expression levels of inflammation-related TLRs, NLRP3 inflammasome complex, angiogenic, hypoxia, and TGF-β/Smads. This model effectively mimics psoriatic inflammatory responses in HaCaT cells and may serve as a cost-effective tool to evaluate the anti-psoriatic potential of new drug candidates. © 2025 Elsevier B.V., All rights reserved.
Protective Effects of Quercetin Against 3.5 GHz RF Radiation-Induced Thyroid Dysfunction and Oxidative Stress in Rats
(Taylor & Francis inc, 2025) Bektas, Hava; Akgun, Burcu Buse Bese; Cakir, Serife; Dogu, Semih; Ahnas, Bedia
The global expansion of 5 G communication networks has heightened concerns about the biological effects of high-frequency radiofrequency (RF) radiation, particularly on endocrine organs such as the thyroid gland. This study investigated the effects of 3.5 GHz RF radiation on thyroid hormone levels and oxidative stress markers in male Wistar rats and assessed the potential protective role of quercetin, a natural antioxidant. Twenty-eight rats were randomly assigned to four groups: Sham, RF, Quercetin, and RF + Quercetin. RF exposure was administered at 3.5 GHz (2 W) for 2 hours/day, 5 days/week, for 30 days. Quercetin (20 mg/kg) was administered intraperitoneally. Serum levels of T3, T4, and TSH, as well as thyroid tissue levels of TAS, TOS, GSH, and MDA, were analyzed using ELISA. RF exposure significantly decreased T3 and T4, increased TSH, elevated MDA and TOS, and reduced TAS and GSH levels. Quercetin treatment showed trends toward reversing some of these effects, although not all changes reached statistical significance. SAR simulations confirmed higher energy absorption in the thyroid region (average SAR: 1.128 W/kg). These findings suggest that 3.5 GHz RF radiation may impair thyroid function and redox homeostasis, and that quercetin may exert limited biochemical protection, though further studies are needed to confirm its efficacy. Further long-term molecular studies are warranted to elucidate the mechanisms involved.