Browsing by Author "Uyanikgil, Yigit"

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Caffeine Mitigates Tamoxifen-Induced Fatty Liver in Wistar Rats
(Acta Cirurgica Brasileira, 2024) Sezgin, Yasin; Bora, Ejder Saylav; Arda, Duygu Burcu; Uyanikgil, Yigit; Erbas, Oytun
Purpose: Tamoxifen, a widely used drug for breast cancer treatment, is associated with adverse effects on the liver, including the development of fatty liver. This study aimed to investigate the potential protective effect of caffeine against tamoxifen-induced fatty liver in Wistar rats. Methods: Rats were divided into normal control, tamoxifen + saline, and tamoxifen + caffeine. Plasma samples were assessed for biochemical markers related to oxidative stress, inflammation, liver function, and cell damage. Additionally, liver histopathology was examined to quantify the extent of fatty infiltration. Results: In the tamoxifen + saline group, elevated levels of plasma malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-alpha), alanine aminotransferase (ALT), cytokeratin 18, and soluble ST2 were observed compared to the normal control group, indicating increased oxidative stress, inflammation, and liver injury (p < 0.01). Moreover, histopathological examination revealed a significant increase in fatty infiltration (p < 0.001). However, in the tamoxifen + caffeine group, these markers were markedly reduced (p < 0.05, p < 0.01), and fatty infiltration was significantly mitigated (p < 0.001). Conclusion: The findings suggest that caffeine administration attenuates tamoxifen-induced fatty liver in rats by ameliorating oxidative stress, inflammation, liver injury, and cell damage. Histopathological evidence further supports the protective role of caffeine. This study highlights the potential of caffeine as a therapeutic intervention to counter tamoxifen-induced hepatic complications, contributing to the optimization of breast cancer treatment strategies.
Imiquimod-Induced Psoriasis-Like Inflammation Model in Calcium-Differentiated Human Keratinocytes Mimics Psoriasis-Associated Biomolecules and Signaling Pathways
(Springer, 2025) Cakir, Mustafa; Keskin, Seda; Uyanikgil, Yigit; Cakir, Serife; Acikgoz, 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-beta/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-beta/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.