Araştırmacılar(15)
Birim yayınları
305 →- ArticleYayıncıda açık erişim2026In vitro evaluation of the antimicrobial, antioxidant, and cytotoxic effects of Zingiber officinale Roscoe ethanolic extract on A2780 ovarian cancer cells
Gunay, Murat; Akyüz, Sümeyye; Akyüz, Emrullah
Aim: To evaluate the in vitro antimicrobial, antioxidant, and anticancer activities of the ethanol extract obtained from Zingiber officinale Roscoe rhizomes (ZRE) against the A2780 ovarian cancer cell line. Materials and Methods: Antimicrobial activity was assessed using disk diffusion and broth microdilution methods. Antioxidant capacity was determined by DPPH and ABTS radical scavenging assays. Anticancer effects were investigated via the XTT cell viability assay. Results: The highest antimicrobial activity was observed against Staphylococcus aureus (16,67±0,57 mm, MIC 64 μg/mL) and Candida albicans (18,67±0,57 mm, MIC 64 μg/mL). Strong, concentration-dependent antioxidant activity was detected in both DPPH and ABTS assays. The IC₅₀ values in the A2780 cell line were determined to be 185±12 μg/mL at 24h and 92±8 μg/mL at 48h. Conclusion: ZRE exhibited notable antimicrobial activity, potent antioxidant capacity, and cytotoxic effects. The originality of this study lies in the simultaneous investigation of ZRE’s multifaceted biological activities.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2026Comprehensive MEFV Variant Spectrum in Pediatric Patients with Suspected Familial Mediterranean Fever: A Whole-Gene Sequencing Study
Gunay, Murat; Demir, Abdussamed Yasin; Yeter, Bahtinur
Objective: To determine the Mediterranean Fever (MEFV) variant spectrum using whole-gene next-generation sequencing (NGS) in pediatric cases with suspected Familial Mediterranean Fever (FMF). Methods: This retrospective cross-sectional study included 471 pediatric cases referred for MEFV analysis. All exons were analyzed using NGS, and variants were classified according to American College of Medical Genetics and Genomics criteria. Results: At least one MEFV variant was detected in 59.4% of cases. A total of 23 variants were identified, predominantly in exon 10 (43.5%) and exon 2 (34.8%). The most frequent variants were R202Q (43.3%), E148Q (16.3%), and M694V (13.7%). A low-frequency variants of uncertain significance, G150R, was detected in one case. Heterozygous genotypes were the most common (59.6%). Conclusion: Whole-gene sequencing enables the detection of both common and rare MEFV variants that may be missed by limited mutation panels. However, frequently detected variants, such as R202Q, require careful interpretation because of their high population frequency and controversial pathogenicity.
RDL Kalıcı Kaydıİncele - ArticleYayıncıda açık erişim2026Neuroendocrine effects of exogenous adropin administration on the hypothalamic pituitary testicular axis in male rats
Eraslan, Ersen; Tanyeli, Ayhan; Güler, Mustafa Can; Özbek Bilgin, Aslı; Ekinci Akdemir, Fazile Nur; Polat, Elif; Çomakli, Selim; Kurt, Nezahat; Bal Taştan, Tuğba
Background/aim: Obesity impairs male fertility through metabolic dysfunction, oxidative stress, and disruption of the hypothalamic– pituitary–testicular (HPT) axis. Adropin (ADR), a peptide hormone whose circulating levels are reduced in obesity, plays emerging roles in metabolic homeostasis; however, its involvement in reproductive endocrine regulation remains unclear. The present study was conducted in healthy, nonobese male rats and aimed to investigate the neuroendocrine and testicular effects of exogenous ADR administration, focusing on circulating reproductive hormones, hypothalamic regulatory peptides, and testicular antioxidant pathways. Materials and methods: Thirty-two male Wistar rats were randomized into control, sham, low-dose ADR (4 μg/kg/day), and high-dose ADR (40 μg/kg/day) groups and treated for 10 days. An enzyme-linked immunosorbent assay (ELISA) was used to measure circulating gonadotropins, testosterone, inhibin B, and activin A. Hypothalamic gonadotropin-releasing hormone (GnRH) and kisspeptin expression, and testicular superoxide dismutase 1 (SOD1) localization were assessed by immunohistochemistry. Brain and testis morphology were examined histologically. Results: High-dose ADR administration was associated with increased hypothalamic GnRH and kisspeptin expression, accompanied by reduced circulating LH levels, while FSH concentrations remained unchanged. Testosterone and inhibin B levels were higher, whereas activin A levels were lower, in the high-dose ADR group compared with controls. ADR administration was also associated with enhanced testicular SOD1 immunoreactivity and dose-dependent reductions in body weight. No overt histopathological alterations were observed in the cerebral cortex or testicular tissue. Conclusion: In healthy, nonobese male rats, exogenous ADR administration was associated with changes in central neuroendocrine markers and testicular antioxidant responses without overt histopathological alterations. These findings do not demonstrate improvements in fertility but suggest that ADR may be involved in pathways linking metabolic signals with reproductive endocrine regulation. The potential relevance of these observations to obesity-associated male reproductive dysfunction remains hypothesis-generating and requires confirmation in appropriate disease models and functional reproductive studies.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2026Effects of adenosine triphosphate and reduced glutathione on biochemical, histopathological and immunofluorescence alterations associated with atezolizumab-induced cardiac tissue injury
Yasar, Yesim Kaya; Sezgin, Esra Tuba; Suleyman, Bahadir; Mammadov, Renad; Ozkaraca, Mustafa; Gungor, Ali; Coban, Taha Abdulkadir; Suleyman, Halis
Background – In this study, the potential protective effects of adenosine triphosphate (ATP) and glutathione (GSH) against atezolizumab-induced cardiac injury in rat heart tissue were investigated. Methods – A total of 24 male albino Wistar rats were used in the experiment. The animals were divided into four groups: healthy group adenosine triphosphate + atezolizumab (ATAZ), GSH + atezolizumab (GHAZ), and atezolizumab alone (ATZ). ATP was administered intraperitoneally at a dose of 4 mg/kg, while GSH was administered orally at a dose of 200 mg/kg for 7 days. Atezolizumab was administered intraperitoneally to the experimental groups at a dose of 10 mg/kg twice weekly. At the end of the experiment, malondialdehyde total glutathione (tGSH), superoxide dismutase catalase, interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels in heart tissues were measured using biochemical methods. In addition, histopathological and immunofluorescence examinations were performed. Results – The results showed that oxidative stress and inflammation markers increased, whereas antioxidant parameters decreased in the atezolizumab-treated group. ATP and GSH administration significantly attenuated these changes and exerted protective effects on cardiac tissue. Conclusion – Overall, ATP and GSH ameliorated the biochemical, histopathological, and immunofluorescence changes associated with atezolizumab-induced cardiac injury in this experimental model.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2026Pathophysiology of sildenafil-induced ocular toxicity in rats and treatment
Cicek, Ibrahim; Caliskan, Busra; Yavuzer, Bulent; Altuner, Durdu; Tastan, Tugba Bal; Coban, Taha Abdulkadir; Karatas, Ezgi; Suleyman, Halis
RESULTS: Sildenafil increased oxidant (malondialdehyde) levels and decreased antioxidant levels (total glutathione, superoxide dismutase, catalase) in rat ocular tissues and caused severe oxidative stress. In addition, sildenafil has been shown histopathologically to cause oxidative damage in retinal layers. ATP treatment suppressed oxidative stress and attenuated histopathological damage in the retinal layers. CONCLUSION: ATP protects retinal tissue against sildenafil-induced ocular oxidative damage in rats and may contribute to the development of novel approaches to prevent or treat this damage.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2026Comparative Protective Effects of ATP and TPP Against Olaparib-Induced Ovarian Injury in Rats: Insights from Biochemical Parameters, Histopathology, and IRE1α, Cleaved Caspase-3, LC3B, and NF-κB p65 Double Immunofluorescence
Paltaci, Seyma Ilayda; Yilmaz, Nesrin; Kozali Uzun, Sukran; Yavuzer, Bulent; Coban, Taha Abdulkadir; Ozkaraca, Mustafa; Gungor, Ali; Yaqubov, Kamandar; Suleyman, Halis
Background: Olaparib is a poly(ADP-ribose) polymerase (PARP) inhibitor used to treat several malignancies. Previous studies have reported that olaparib may induce ovarian injury by elevating reactive oxygen species and impairing cellular energy homeostasis. ATP is a central regulator of intracellular energy balance and antioxidant defense, whereas thiamine pyrophosphate (TPP), the active form of vitamin B1, supports ATP biosynthesis and possesses antioxidant and anti-inflammatory properties. This study compared the protective effects of ATP and TPP against olaparib-induced ovarian injury in rats. Methods: Twenty-four female Wistar albino rats were randomly assigned to four groups (n=6 each): healthy control (HG), olaparib-only (OLP), ATP plus olaparib (ATOL), and TPP plus olaparib (TPOL). Olaparib (100 mg/kg, orally, twice daily), ATP (5 mg/kg, intraperitoneally, once daily), and TPP (25 mg/kg, intraperitoneally, once daily) were administered for 14 consecutive days. Ovarian tissue levels of oxidant (MDA), antioxidants (tGSH, SOD, CAT), and pro-inflammatory cytokine (IL-6) were determined. Tissue specimens underwent histopathological (follicular and parenchymal degeneration) and double immunofluorescence analyses (IRE1α, cleaved Caspase-3, LC3B, and NF-κB p65 immunopositivity). Results: Olaparib significantly increased oxidant and pro-inflammatory cytokine levels and decreased antioxidant levels. Histopathology revealed severe follicular and parenchymal degeneration, and immunofluorescence analysis showed significantly increased IRE1α, cleaved Caspase-3, LC3B, and NF-κB p65 immunopositivity. Both ATP and TPP pre-treatment significantly attenuated olaparib-induced oxidative stress, inflammatory responses, histopathological injury, and cellular stress marker immunopositivity. ATP demonstrated a more pronounced protective effect than TPP, particularly regarding follicular degeneration suppression and LC3B and NF-κB p65 immunopositivity. Conclusion: Olaparib induced ovarian injury accompanied by oxidative stress, cytokine-mediated inflammation, IRE1α-related endoplasmic reticulum stress, cleaved Caspase-3-related apoptosis, LC3B-related autophagy, and NF-κB-related inflammatory signaling. Both ATP and TPP attenuated olaparib-associated injury, with greater effects for ATP. These findings suggest that maintenance of cellular energy homeostasis may represent a promising strategy for attenuating PARP inhibitor-induced ovarian injury.
RDL Kalıcı Kaydıİncele - ArticleYayıncıda açık erişim2026Direct Relationship Between Heparin Binding to Midkine and Pleiotrophin and the Development of Acute Deep Vein Thrombosis
Aydin, Suna; Polat, İsmail; Tural, Kevser; Duger, Nurullah; Ugur, Kader; Sahin, İbrahim; Aydin, Suleyman; Lee, Do-Youn
Background/Objectives: The underlying molecular mechanisms of deep vein thrombosis (DVT), which continues to be a major global public health concern, remain unclear. A key component of anticoagulant therapy, heparin (HP) interacts with heparin-binding growth factors including pleiotrophin (PTN) and midkine (MK), both of which have basic amino acid-rich domains that have a strong affinity for HP. The purpose of this study was to determine if changes in the levels of circulating HP, MK, and PTN are linked to the onset of acute DVT. Methods: Thirty patients diagnosed with acute DVT by venous Doppler ultrasonography (VDU) and 28 healthy controls with normal VDU findings were enrolled. Serum HP, MK, and PTN concentrations were measured using ELISA. In DVT patients, blood samples were obtained before and after routine subcutaneous low-molecular-weight heparin treatment; controls provided a single blood sample. ROC curve analysis was used to assess diagnostic performance. Results: Prior to treatment, patients with acute DVT exhibited significantly lower serum HP levels (p < 0.05) and significantly higher MK and PTN levels compared with healthy controls (both p < 0.05). Following heparin administration, serum HP levels increased significantly (p < 0.05), while MK and PTN levels showed a decreasing trend that did not reach statistical significance (p > 0.05). ROC curve analysis demonstrated limited diagnostic performance for HP (sensitivity 10.3%, specificity 68.8%), PTN (62.1%, 54.2%), and MK (82.8%, 35.4%). Conclusions: Decreased circulating HP and increased MK and PTN levels are characteristics of acute DVT that may indicate endogenous HP sequestration through binding to these growth factors. This imbalance could lead to less free HP being available, which would encourage the formation of thrombus. Therapeutic approaches that target MK- and PTN-mediated HP interactions may constitute a unique approach for the therapy of acute DVT, as evidenced by the partial normalization seen after exogenous heparin delivery.
RDL Kalıcı Kaydıİncele - ArticleYayıncıda açık erişim2026Protective Role of Adenosine Triphosphate Against Tamoxifen-Induced Retinal Toxicity in a Rat Model
Karatas, Ezgi; Yavuzer, Bulent; Koksaldi, Seher; Kayabasi, Mustafa; Sezgin, Esra Tuba; Sarigul, Cengiz; Demir, Ozlem; Suleyman, Bahadir; Suleyman, Halis
Background and Objectives: Tamoxifen, a cornerstone selective estrogen receptor modulator in breast cancer therapy, is increasingly recognized to be associated with retinal toxicity characterized by mitochondrial dysfunction, oxidative stress, lipid peroxidation, and oxidative DNA injury. By targeting mitochondrial bioenergetic dysfunction and redox disequilibrium, adenosine triphosphate (ATP) emerges as a biologically plausible candidate for retinal cytoprotection. This study aimed to evaluate the protective effect of ATP against tamoxifen-induced retinal toxicity in a rat model. Materials and Methods: Twenty-four male albino Wistar rats were randomly assigned to four groups: healthy control (HG), ATP-alone (ATPG, 4 mg/kg, intraperitoneally), tamoxifen-alone (TAMG, 5 mg/kg, orally), and tamoxifen plus ATP-treated (ATAG; ATP, 4 mg/kg, intraperitoneally; tamoxifen, 5 mg/kg, orally). Treatments were administered once daily for 30 days. Oxidative stress markers (malondialdehyde, total glutathione), antioxidant enzyme activities (superoxide dismutase, catalase), and oxidative DNA damage (8-hydroxy-2′-deoxyguanosine) were assessed in ocular tissues. Retinal histopathological evaluation included hematoxylin–eosin staining with semiquantitative assessment of edema, vascular congestion, polymorphonuclear leukocyte infiltration, and cytoplasmic vacuolization, together with quantitative measurements of retinal layer thicknesses and ganglion cell layer (GCL) cell counts. Results: Tamoxifen administration induced marked oxidative stress, antioxidant depletion, and increased oxidative DNA damage in ocular tissues, accompanied by significant thickening of retinal layers, reduced GCL cell counts, and pronounced disruption of retinal architecture. By comparison, ATP co-administration significantly suppressed lipid peroxidation and restored antioxidant defenses, thereby reducing oxidative DNA damage and preserving retinal structural integrity, as reflected by partial normalization of retinal layer thicknesses, preservation of GCL cell counts, and the presence of only mild residual edema. Conclusions: These findings indicate that ATP attenuates tamoxifen-induced retinal toxicity by supporting mitochondrial energy balance and redox homeostasis. Accordingly, ATP administration may represent a promising protective approach for reducing retinal injury associated with long-term tamoxifen therapy.
RDL Kalıcı Kaydıİncele - ArticleYayıncıda açık erişim2026Liraglutide Attenuates Multiorgan Oxidative, Astroglial, and Mitochondrial Stress Responses in Thioacetamide-Induced Hepatic Encephalopathy
Bilgin, Yasin; Sari, Fatih Mehmet; Cicek, Betul; Kurt, Engin; Ozkaraca, Mustafa; Gungor, Ali; Kurt, Nezahat; Bilgin, Asli Ozbek
Hepatic encephalopathy (HE) is a complex complication of liver failure involving oxidative stress, astroglial activation, mitochondrial dysfunction, and multiorgan disturbances along the gut–liver–brain axis. This study investigated the therapeutic effects of liraglutide (LIRA) in a thioacetamide (TAA)-induced rat model of HE. Thirty male Sprague–Dawley rats were assigned to control, TAA, and TAA+LIRA 100, 200, or 400 µg/kg groups. HE was induced with TAA (200 mg/kg, intraperitoneally) for three consecutive days, followed by subcutaneous LIRA treatment for 14 days. Serum biochemical parameters, tissue oxidative and inflammatory markers, histopathology, and Nrf2, MFN2, AKT1, mTOR, GFAP, and VEGFA immunoreactivity were evaluated. TAA caused marked hepatic and cerebral structural injury, increased serum and brain glutamine concentrations, disrupted redox homeostasis, elevated MPO activity, and increased cerebral GFAP and multiorgan VEGFA immunoreactivity. LIRA partially improved hepatic and cerebral histopathology, reduced glutamine disturbances, attenuated selected oxidative, nitrosative, and inflammatory alterations, and modulated Nrf2, MFN2, AKT1, mTOR, GFAP, and VEGFA immunoreactivity in a tissue- and dose-specific manner. The 200 µg/kg dose produced the most consistent overall improvement, whereas the 400 µg/kg dose was less favorable for several endpoints. LIRA may therefore alleviate multiorgan stress associated with experimental HE, although further studies are required to confirm functional and mechanistic relevance.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2026Assessment of methylene blue and NAD on LPS-induced acute brain injury: effects on neuroinflammation, oxidative stress, and blood–brain barrier integrity in a rat endotoxemia model
Doganay, Songul; Üstündağ, Hilal; Erbaş, Elif; Yanar, Sevinc; Hayme, Serhat; Kurt, Nezahat
Sepsis-induced brain dysfunction remains a significant challenge with limited therapeutic options, warranting exploration of multi-target approaches. Methylene blue (MET) is a phenothiazine derivative with mitochondrial-enhancing and electron transport chain regulatory properties, while nicotinamide adenine dinucleotide (NAD) serves as a crucial cofactor in cellular energy metabolism and redox reactions. This study investigated the therapeutic effects of MET and NAD, individually and in combination, in lipopolysaccharide (LPS)-induced sepsis model. Male Sprague–Dawley rats (n = 35) were randomized into five groups: control, LPS (8 mg/kg), LPS + NAD (250 mg/kg), LPS + MET (15 mg/kg), and LPS + NAD + MET. Brain tissues were analyzed for oxidative stress, inflammation, and blood–brain barrier integrity. The combination therapy demonstrated the most pronounced improvements across clinical parameters, antioxidant capacity evidenced by significantly elevated superoxide dismutase levels (p < 0.001) and cerebral histopathological outcomes. It also significantly reduced myeloperoxidase activity (p < 0.001) compared to the LPS group. Pro-inflammatory cytokines IL-6 and IL-8 were significantly decreased in both MET and NAD monotherapy groups (p < 0.05), while TNF-α showed a decreasing trend without statistical significance. Brain-derived neurotrophic factor levels were maintained in the combination group, comparable to controls, while TGF-β showed differential modulation across treatment groups. Immunohistochemical analysis revealed LPS-induced blood–brain barrier disruption, evidenced by reduced occludin expression (p < 0.01), increased aquaporin-4 expression in perivascular astrocytic end-feet (p < 0.05), and elevated glial fibrillary acidic protein reactivity in protoplasmic astrocytes (p < 0.01). In conclusion, MET and NAD individually provided significant protection against LPS-induced brain injury by reducing neuroinflammation, oxidative stress, and neuronal damage. The combined treatment offered incremental benefits in certain outcomes. These findings suggest that both agents may have therapeutic potential in SAE.
RDL Kalıcı Kaydıİncele
Tam Kayıt
| Alan | Değer | Dil |
|---|---|---|
| dc.date.accessioned | 2026-10-20T15:26:06.310906720Z | |
| dc.date.available | 2026-10-20T15:26:06.310906720Z | |
| dc.identifier.uri | https://rdlopen.rawdatalibrary.net/r/ebyu/22879 | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.title | Tıbbi Biyokimya Anabilim Dalı | tr |
| dc.title | Department of Medical Biochemistry | en |
| dspace.entity.type | OrgUnit | |
| organization.identifier.code | tip-biyokimya | |
| organization.unitType | department | |
| rdl.unit.alias | biochem |
