Browsing by Author "Seker, Ugur"

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An Examination of the Effects of Propolis and Quercetin in a Rat Model of Streptozotocin-Induced Diabetic Peripheral Neuropathy
(Mdpi, 2024) Tueredi, Sibel; Celik, Hakim; Dagli, Seyda Nur; Taskin, Seyhan; Seker, Ugur; Deniz, Mustafa
The purpose of this study was to reveal the combined effects of propolis (P) and quercetin (Q) against diabetic peripheral neuropathy developing with streptozotocin-induced diabetes in rats. Sixty-four adult male rats were divided into eight equal groups: control, P (100 mg/kg/day), Q (100 mg/kg/day), P + Q (100 mg/day for both), diabetes mellitus (DM) (single-dose 60 mg/kg streptozotocin), DM + P, DM + Q, and DM + P + Q. The rats were sacrificed, and blood and sciatic nerve tissues were collected. Blood glucose and malondialdehyde (MDA) levels increased, while IL-6 and total antioxidant status decreased in the DM group (p = 0.016 and p = 0.047, respectively). Ultrastructural findings showed degeneration of the axon and myelin sheath. The apoptotic index (AI %), TNF-alpha, and IL-1 beta immunopositivity increased significantly in the DM group (p < 0.001). Morphological structures approaching those of the controls were observed in the DM + P, DM + Q, and DM + P + Q groups. Morphometric measurements increased markedly in all treatment groups (p < 0.001), while blood glucose and MDA levels, AI (%), TNF-alpha, and IL-1 beta immunopositivity decreased. In conclusion, the combined effects of propolis and quercetin in diabetic neuropathy may provide optimal morphological protection with neuroprotective effects by reducing hyperglycemia, and these may represent a key alternative supplement in regenerative medicine.
The Involvement of the Serotonergic System in Ketamine and Fluoxetine Combination-Induced Cognitive Impairments in Mice
(Ataturk Univ, 2024) Uyar, Emre; Erdinc, Meral; Kelle, Lker; Erdinc, Levent; Seker, Ugur; Nergiz, Yusuf
Background: Gluta mater gic N-methyl-D-aspartate (NMDA) receptors play vital roles in memory formation. Changes in the activity of these receptors influence memory processes. Ketamine is a noncompetitive NMDA receptor antagonist drug with promising mood-altering and pain-reducing effects ff ects in low doses. These effects ff ects are believed to be related to altered serotonergic transmission. Methods: The present study investigated the involvement of the serotonergic system in low-dose ketamine administrations' effects ff ects on memory acquisition, consolidation, and retrieval processes. Sixty-four male BALB/c mice were used in this experiment and separated into 8t groups. Mice were treated subchronically with a selective serotonin reuptake inhibitor, fluoxetine, and a serotonin depletion agent, p-chlorophenylalanine (pCPA). A serotonin antagonist, methiothepin, and ketamine were acutely administered 60 minutes before or after the behavioral tests. A passive avoidance (PA) test measured emotional memory acquisition, consolidation, and retrieval processes. Hippocampi malondialdehyde (MDA) levels were analyzed, and histopathological examinations were performed. Results: Ketamine alone did not significantly affect ff ect memory encoding processes in the PA test, while the ketamine-fluoxetine combination disrupted memory consolidation. Fluoxetine negatively affected ff ected the memory acquisition process, which was normalized during the consolidation and retrieval trials. Drug applications did not significantly alter hippocampal MDA levels. In all ketamine-applied groups, histopathologic alterations were evident. Conclusion: Low-dose ketamine administration induces neurodegeneration, and it also impairs memory functions when combined with fluoxetine, indicating increased serotonergic transmission may be involved in the memory-impairing and neurotoxic effects ff ects of ketamine.
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.
Neuroprotective Potential of a Novel Soluble Guanylate Cyclase Stimulator the Riociguat Alone or in a Combination Manner With Resveratrol in Experimental Stroke Model in Rats
(Soc Chilena Anatomia, 2024) Aslanoglu, Baris; Kaya, Seval; Gunara, Sezer Onur; Atlas, Burak; Seker, Ugur; Guzel, Baris Can; Turan, Yahya
In this study we aimed to examine the effect of novel vasodilatory drug Riociguat co-administration along resveratrol to recover neurodegeneration in experimental stroke injury. For that purpose, thirty-five adult female rats were divided into groups five (Control, MCAO, MCAO + R, MCAO + BAY, MCAO + C) of seven animals in each. Animals in Control group did not expose to any application during the experiment and sacrificed at the end of the study. Rats in the rest groups exposed to middle cerebral artery occlusionO) (MCAinduced ischemic stroke. MCAO + R group received 30 mg/kg resveratrol, and MCAO + BAY group received 10 mg/kg Riociguat. The MCAO + C group received both drugs simultaneously. The drugs were administered just before the reperfusion, and the additional e doses weradministered 24h, and 48h hours of reperfusion. All animals in this study were sacrificed at the 72nd hour of experiment. Total brainsreceived were for analysis. Results of this experiment indicated that MCAO led to severe injury in cerebral structure. Bax, IL-6 and IL-1 ss levelstissue were upregulated, but anti-apoptotic Bcl-2 immunoexpression was suppressed (p<0.05). In resveratrol and Riociguat treated animals, the neurodegenerations and apoptosis and inflammation associated protein expressions were improved compared to MCAO group, mosbut the success was obtained in combined treatment exposed animals in MCAO + C group. This study indicated that the novel solubleate guany cyclase stimulator Riociguat is not only a potent neuroprotective drug in MCAO induced stroke, but also synergistic administratio of Riociguat along with resveratrol have potential to increase the neuroprotective effect of resveratrol in experimental cerebral strokeosed rats.
Regulation of Stat3 and Nf-Κb Signaling Pathways By Trans-anethole in Testicular Ischemia-Reperfusion Injury and Its Gonadoprotective Effect
(Mre Press, 2024) Seker, Ugur; Gokce, Yasin; Kati, Bulent; Yuksel, Meral; Guzel, Baris Can; Shokoohi, Majid
Testicular ischemia reperfusion (I/R) injury is a significant urological problem where clinical interventions may be inadequate, and the antioxidants might be potential co-treatment modalities. This study examined the gonadoprotective effect of trans-Anethole in testicular I/R injury. Twenty-eight male rats were divided into four groups. Rats in the I/R, I/R + t100, I/R + t200 groups underwent bilateral testicular I/R injury. The I/R + t100 and I/R + t200 groups received 100 or 200 mg/kg trans-Anethole at the 2nd hour of ischemia. Microscopic evaluations demonstrated that testicular I/R injury leads to severe testicular degeneration. Tissue oxidative stress, pro-apoptotic Bcl-2 associated X (Bax) and Caspase 3, pro-inflammatory Tumor necrosis factor-alpha (TNF-alpha), Interleukin-1 beta (IL-1 beta) and Interleukin 6 (IL-6) cytokines levels were significantly (p < 0.05) upregulated when compared to the Control group. Additionally, transcription factors Signal transducer and activator of transcription 3 (STAT3) and Nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) levels increased significantly (p < 0.05) compared to the Control group. Tissue disrupted parameters in the I/R + t200 group were significantly different (p < 0.05) from the I/R group, contrasting with the slight improvement in the I/R + t100 group. The STAT3 and NF-kappa B expression levels in the I/R + t200 group were significantly suppressed (p < 0.05) compared to the I/R group. In conclusion, our study indicates that trans-Anethole could enhance gonadoprotective activity in testicular I/R injury, potentially involving transcription factors STAT3 and NF-kappa B. However, before the consumption of trans-Anethole-containing natural or manufactured goods, the potential benefits and side effects should be carefully evaluated.
Safety Analysis of Different Intensities of Elf-Pemf in Terms of Apoptotic, Inflammatory, and Transcription Factor Nf-Κb Expression Levels in Rat Liver
(Kare Publ, 2024) Gokce, Yasin; Seker, Ugur; Ozoner, Merve Pekince
Background and Aim: The purpose of this research was to ascertain how exposure to extremely low-frequency pulsed electromagnetic fields (ELFPEMFs) at varying intensities affects apoptosis-related protein expression levels and liver morphology in rats. Materials and Methods: In this experimental study, 40 Wistar albino rats were randomly divided into 4 groups, with 10 animals in each group: Control, Sham, 1 milli Tesla (1mT), and 5 mT groups. The control group did not expose any application during the experiment. Animals in the sham group were placed into the closed ELF-PEMF exposure environment, but the device was kept closed. The rats in the 1mT and 5mT groups were placed into a closed ELF-PEMF exposure environment, and the magnetic field application was applied 5 days a week for 4 hours a day for 8 weeks. At the end of the study, the animals were sacrificed, and their liver tissues were examined morphologically, and the expression levels of proteins related to apoptosis and inflammation in these tissues were analyzed. Results: Our results indicated that ELF-PEMFs did not lead to any exact morphological alterations in the groups. Tissue apoptotic Bax and Caspase the control group. Additionally, pro-inflammatory TNF-alpha and transcription factor NF-kappa B in the 1mT and 5mT groups were similar (p>0.05) to each other and the control group. ELF-PEMF in rats.