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    The M1/M2 Macrophage Polarization and Hepatoprotective Activity of Quercetin in Cyclophosphamide-Induced Experimental Liver Toxicity
    (Wiley, 2025) Seker, Ugur; Uyar, Emre; Gokdemir, Gul Sahika; Kavak, Deniz Evrim; Irtegun-Kandemir, Sevgi
    Background: Chemotherapy drugs may lead to hepatic injury, which is considered one of the limitations of these drugs. Objectives: The aim of this study was to evaluate the effect of quercetin (QUE) on M1/M2 macrophage polarization and hepatoprotective effect in cyclophosphamide (CTX)-induced liver toxicity. Methods: Twenty-four mice were divided into four groups (Control, QUE, CTX, CTX + QUE). The CTX and CTX + QUE groups received 200 mg/kg CTX. The animals in the QUE and CTX + QUE groups received 50 mg/kg QUE. All animals were sacrificed, and serum and liver samples were used for laboratory analyses. Results: Examinations indicated that CTX exposure led to disruption of liver functions and morphological degenerations. Tissue pro-apoptotic Bax and caspase 3, pro-inflammatory TNF-alpha and IL-1 beta, transcription factor NF-kappa B, and M1 macrophage polarization marker CD86 were upregulated significant (p < 0.05) in this group. In addition, CTX exposure led to significantly (p < 0.05) upregulation of the Bax/Bcl-2 mRNA ratio and DNA fragmentations. The PCNA-positive hepatic cell ratio and anti-apoptotic Bcl-2 expression are remarkably suppressed (p < 0.05). Immunohistochemical analyses are also indicated that M2 macrophage polarization marker CD163 is slightly but remarkably (p < 0.05) downregulated in the CTX group compared to the Control and QUE groups. The morphological and biochemical disruptions were alleviated in QUE-treated animals in the CTX + QUE group. Liver function test results, apoptosis, inflammatory, transcription factor NF-kappa B, regeneration/proliferation, and apoptotic index results in this group were similar (p > 0.05) to the control and QUE groups. The M1 cell surface marker expression of CD86 is significantly (p < 0.05) downregulated, and M2 macrophage polarization marker expression of CD163 is upregulated significantly (p < 0.05) compared to the CTX group. Conclusions: This study indicates that QUE has the potential to downregulate CTX-induced hepatic injury and regulate M1/M2 macrophage polarization to the M2 side, which indirectly demonstrates activation of anti-inflammatory signalling and tissue repair.
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    mRNA Expression Profile of SFKs and Involvement of SFKs in the Regulation of LPS-Induced Erk1/2 Signaling in PBMCs of Active BD Patients
    (Bentham Science Publ Ltd, 2019) Irtegun-Kandemir, Sevgi; Icen-Taskin, Irmak; Bozkurt, Mehtap; Kalkanli-Tas, Sevgi
    Background: Behcet's Disease (BD) is a multisystemic inflammatory disorder affecting large vessels, lungs joints, gastrointestinal and neurological systems. The pathogenesis of BD remains poorly understood. Identifying the key signaling pathway is crucial for a complete understanding of the pathogenesis of BD. Objective: The aim of this study was to determine mRNA expression level of Src family kinases (SFKs) members and their involvement in lipopolysaccharide (LPS)-induced mitogen-activated protein kinases (MAPKs) regulation in peripheral blood mononuclear cells (PBMCs) of active BD patients. Methods: Twenty- five active BD patients and twenty-five healthy controls were included in the study. PBMCs were isolated from total blood by density gradient centrifugation. The mRNA expression levels of SFKs members were measured by real-time quantitative PCR (RT-qPCR). The effect of SFKs activity on LPS-induced activation MAPKs (Erk1/2, p38 and JNK) was examined by Western blot. Results: The mRNA expression levels of Hck, Src, Lyn, Yes and Fyn were found to be slightly decreased in active BD patients compared to the control subjects, but a slight change in mRNA level of SFKs members did not impact on protein levels and protein activity. LPS-induced Erk1/2 phosphorylation was significantly increased in the absence of SFKs activity in active BD patients. However, inhibition of SFKs activity had no effect on LPS-induced phosphorylation of p38 and JNK in both controls and active BD patients. Conclusion: SFKs downregulate LPS-induced Erk1/2 phosphorylation in PBMCs of active BD patients.
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    TP53 rs1042522 polymorphism and early-onset breast cancer
    (Wolters Kluwer Medknow Publications, 2020) Icen-Taskin, Irmak; Irtegun-Kandemir, Sevgi; Munzuroglu, Omer
    Background: Breast cancer is the leading cause of cancer deaths among women. Early-onset breast cancer is well recognized as it clinically differs from old-age diagnosed breast neoplasms. TP53 rs1042522 polymorphism relates to the risk of breast neoplasms, but this relationship in Turkish early-onset breast cancer patients has not been investigated yet. We aimed to search the relationship between TP53 rs1042522 polymorphism and young Turkish breast cancer patients. Materials and Methods: Ninety-six female breast cancer patients who were <= 40 years of age and 96 healthy controls were enrolled in our study. Participants were genotyped by the hybridization probe system. Results: We identified that the genotype frequencies of rs1042522 were significantly different between controls and cases (P = 0.027). Participants carrying CG genotype had also reduced breast cancer risk (odds ratio = 0.4196, 95% confidence interval: 0.1941-0.9067, P = 0.027). Our results revealed that there is an association between GG and CG + CC genotype groups with progesterone receptor (PgR) status (P = 0.0219). Conclusion: Our findings indicate that the CG genotype is a protective factor against breast neoplasms. No other clinicopathologic parameters except for PgR status were found to be related to rs1042522 polymorphism in young Turkish breast cancer patients.