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Öğe Acrylamide, Applied During Pregnancy and Postpartum Period in Offspring Rats, Significantly Disrupted Myelination by Decreasing the Levels of Myelin-Related Proteins: MBP, MAG, and MOG(Springer/Plenum Publishers, 2024) Uremis, Muhammed Mehdi; Uremis, Nuray; Gul, Mehmet; Gul, Semir; Cigremis, Yilmaz; Durhan, Merve; Turkoz, YusufAcrylamide (ACR) is a colorless, odorless, and water-soluble solid molecule. In addition to being an important industrial material, ACR is found in fried and baked carbohydrate-rich foods. ACR is regarded as a typical axonal neurotoxin that induces neuropathy. The brain is protected from oxidative damage by vitamin E, which is regarded as the most powerful fat-soluble antioxidant vitamin. This study aimed to reveal the toxic effect of ACR on the development of myelin in the brain at the molecular level and to examine whether Vitamin E has a neuroprotective effect on the harmful effect of ACR. The study was started by dividing 40 pregnant rats into 4 groups and after lactation, the study was continued with offspring rats (females and males offspring rats) from each group. Offspring rats were equally divided into Control, Vitamin E, ACR, ACR + Vitamin E groups. Following the ACR administration, the Water Maze test was applied to evaluate cognitive function. To evaluate the level of demyelination and remyelination, MBP, MAG, and MOG proteins and mRNA levels were performed. In addition, the degeneration of myelin and glial cells was examined by immunohistochemistry and electron microscopic analysis. Analysis results showed that ACR administration decreased gene and protein levels of myelin-related proteins MBP, MAG, and MOG. The findings were confirmed by histopathological, immunohistochemical, and microscopic examinations. The application of vitamin E improved this negative effect of ACR. It has been observed that ACR may play a role in the pathogenesis of myelin-related neurodegenerative diseases by causing demyelination during gestation, lactation, and post-lactation. In addition, it has been understood that vitamin E supports myelination as a strong neuroprotective vitamin against the toxicity caused by ACR. Our research results suggest that acrylamide may play a role in the etiopathogenesis of demyelinating diseases such as multiple sclerosis in humans since fast-food-type nutrition is very common today and people are chronically exposed to acrylamide.Öğe Alamandine alleviates methotrexate-induced nephrotoxicity in rats by targeting oxidative stress and inflammation(2023) Yıldız, Azibe; Aras, Muhammed Yasir; Gunata, Mehmet; Durhan, Merve; Polat, Seyhan; Parlakpınar, Hakan; Cigremis, YilmazAim: Nephrotoxicity due to the use of methotrexate (Mtx) is one of the most important problems associated with chemotherapy. Oxidative stress and inflammation are the major pathomechanisms of Mtx-induced nephrotoxicity. Alamandine (Ala), a new member of the renin-angiotensin system (RAS), is an important peptide with antioxidant and antiinflammatory capacities. In this study, it was investigated whether Ala ameliorates Mtxinduced kidney damage by reducing oxidative stress and inflammation. Materials and Methods: Male Wistar albino rats were assigned into three groups: control group, Mtx group, and Mtx+Ala group. At the end of the experiment, kidney tissues were quickly removed. Glutathione (GSH) and malondialdehyde (MDA) levels were measured to determine the oxidative state in kidney tissues. In addition, tissue samples were assessed as histopathological and immunohistochemical for heat shock protein 60 (HSP60), caspase-3, tumor necrosis factor-? (TNF-?), and receptor-interacting protein kinase-3 (RIPK3). Results: Mtx treatment resulted in reduced GSH content, elevated MDA level, increased heat shock protein 60 (HSP60), and caspase-3 expression. These changes in kidney tissues of rats treated with Mtx triggered oxidative stress characterized by apoptosis and kidney damage. Mtx also markedly increased the expression of TNF-?, an inflammation marker, and RIPK3, a marker of necroptosis. However, Ala administration significantly alleviated Mtx-induced kidney damage by reducing apoptosis and necroptosis by suppressing oxidative stress and inflammation. Conclusion: Taken together, our results support that Ala treatment can serve as a new and promising therapeutic strategy against Mtx-induced nephrotoxicity.Öğe Cucurbitacin D Inhibits the Proliferation of HepG2 Cells and Induces Apoptosis by Modulating JAK/STAT3, PI3K/Akt/mTOR and MAPK Signaling Pathways(Bentham Science Publ Ltd, 2022) Uremis, Muhammed Mehdi; Uremis, Nuray; Tosun, Emir; Durhan, Merve; Cigremis, Yilmaz; Baysar, Ahmet; Turkoz, YusufBackground: Cucurbitacin D (CuD) is a natural compound that can be isolated in various plant families, mainly from Ecballium elaterium (L.) A. Rich. (E. elaterium). It is a triterpenoid with a broad spectrum of biological activity, including anti-cancer properties. Hepatocellular carcinoma, the aggressive type of liver cancer, is an important public health problem worldwide. Objective: In the present study, we investigated the anticancer effect of CuD treated at different doses on the HepG2 cell line and the underlying mechanism in vitro. Methods: CuD was isolated from the fruit juice of E. elaterium plant, and quantitative analysis was performed using high-performance liquid chromatography. The cell viability effect of purified CuD was determined by the MTT test, and also cell apoptosis and cell cycle arrest effects were determined by flow cytometry. DNA damage was evaluated with the comet test. Proteins and genes involved in PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 signaling pathways were evaluated by western blot and qRT-PCR. Results: CuD showed both antiproliferative and cytotoxic effects against the HepG2 cell line in a dose and time-dependent manner. It was observed that CuD induced apoptosis and blocked the cell cycle in HepG2 cells. It was observed that the expressions of genes and some proteins that play a key role in PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 cascades were dose-dependently down-regulated and led to activatation of the apoptotic pathway. Conclusion: All these results show promise that CuD may have a therapeutic effect in hepatocellular carcinoma.Öğe The Effect of Curcumin on Brain TRPM2 Channel Gene mRNA Expression Level in Experimental Alzheimer's Rat Model Induced by Application of Intracerebroventricular Streptozotocin(Karger, 2018) Durhan, Merve; Tunc, Selahattin; Tekin, Suat; Kaya, Gul Busra; Yildiz, Azibe; Cigremis, Yilmaz[Abstract Not Available]Öğe Effects of caffeic acid phenethyl ester use and inhibition of p42/44 MAP kinase signal pathway on caveolin 1 gene expression and antioxidant system in chronic renal failure model of rats(Taylor & Francis Ltd, 2023) Cigremis, Yilmaz; Ozen, Hasan; Durhan, Merve; Tunc, Selahattin; Kose, EvrenEffects of Caffeic acid phenethyl ester (CAPE) and/or PD98059 (PD) on the gene expression of Caveolin-1 (CAV1) and reduced glutathione (GSH), malondialdehyde (MDA), copper-zinc superoxide dismutase (CuZn-SOD), and catalase (CAT) enzyme activities were investigated in an experimental chronic renal failure model in rats. Eighty Wistar rats were divided into eight groups for a 28-day study: Control, CsA (Cyclosporine A), CsA-V (CsA solvent), CsA + PD (CsA + PD98059), CsA + PD + CAPE, CsA + CAPE, CAPE-V (CAPE solvent), and PD-V (PD98059 solvent). Serum blood urea nitrogen and creatinine levels, as well as histopathological findings indicated the development of renal failure in the CsA group. Kidney GSH levels decreased while MDA levels, CuZn-SOD, and CAT activities increased significantly in the CsA group compared to control indicating oxidative stress. CAV1 gene expression significantly decreased in the CsA group compared to the control. PD98059 and CAPE applications made positive improvements in the levels of the parameters investigated. PD98059 and CAPE applications in CsA given animals increased GSH and CAV1 gene expressions and decreased CuZn-SOD and CAT levels compared to the CsA group. In conclusion, it was shown that PD98059 and CAPE could attenuate the effects of chronic renal failure, and CAV1 is suggested as a therapeutic target and the inhibition of the p44/42 MAPK pathway may be a new approach for the treatment of renal degenerations.Öğe Effects of noopept on cognitive functions and pubertal process in rats with diabetes(Pergamon-Elsevier Science Ltd, 2019) Gurbuz, Perihan; Duzova, Halil; Yildiz, Azibe; Cakan, Pinar; Kaya, Gul Busra; Bag, Harika Gozde Gozukara; Durhan, MerveAim: Type 1 diabetes (T1DM) is a common chronic disease in childhood. Increasing insulin resistance in puberty gives rise to higher doses of insulin usage in treatment. Of this reason new approaches in treatment are needed. Noopept researches suggest it to have anti-diabetic properties. We tried to determine the effects of noopept on pubertal diabetes. Main method: The research was made with 60 prepubertal, 28 day-old, male, Sprague Dawley rats. The rats were divided into randomised 6 groups (n = 10/group). i) Control, ii) Diabetes Control, iii) Noopept Control, iv) Diabetes + Noopept, v) Diabetes + Insulin, vi) Diabetes + Insulin + Noopept. T1DM model was induced by streptozotocin on postnatal 28th day. 0.5 mg/kg noopept and 1 IU insulin were administered intraperitoneally for 14 days. Blood glucose and body weight measurements, puberty follow-up and MWM tests were performed. Hippocampus, hypothalamus and testis were evaluated histologically. Hypothalamic GnRH and kisspeptin were studied immunohistochemically. Serum LH, FSH and insulin, hippocampal homogenate NGF and BDNF levels were determined by ELISA. Key findings: Delayed puberty was normalized by noopept (p < 0.05). Blood glucose levels were lower in noopept-administered diabetic groups (p < 0.05). Noopept decreased HOMA-IR in insulin administered diabetic group (p < 0.05). Number of degenerated cells in hippocampus and testis were higher in diabetes control group when compared with other groups (p < 0.05). GnRH immunoreactivity in Diabetes + Noopept group was increased when compared to insulin + noopept group (p = 0.018). There was no difference in kisspeptin, serum LH, FSH, hippocampal NGF-BDNF levels and spatial learning assessment among groups (p > 0.05). Significance: Noopept may have positive effect in treatment of pubertal diabetes.Öğe Effects of Noopept on Hippocampal NGF and BDNF Levels and Cognitive Functions of Prepubertal Rats with Streptozotocin-Induced Diabetes(Karger, 2018) Gurbuz, Perihan; Duzova, Halil; Kaya, Gul Busra; Cakan, Pinar; Durhan, Merve[Abstract Not Available]Öğe Effects of noopept on hippocampal ngf and bdnf levels and cognitive functions of prepubertalrats with streptozotocin-ınduced diabetes(KARGER, ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND, 2018) Gürbüz, Perihan; Düzova, Halil; Kaya, Gül Büşra; Çakan, Pınar; Durhan, MerveÖğe İntraserebroventriküler streptozotosin uygulamasıyla oluşturulan deneysel alzheimer sıçan modelinde kurkumin'in beyin trpm2 kanal protein geni ifadesine etkisi(İnönü Üniversitesi, 2017) Durhan, MerveAmaç: Streptozotosin sıçan beyninde insüline direnç oluşturarak Alzheimer benzeri patoloji oluşturmaktadır ve deneysel sıçan modeli olarak başarılı kabul edilmektedir. Kurkuminin deneysel Alzheimer sıçan modellerinde oksidatif stresi ve amiloid plaklarını azaltarak koruyucu ve tedavi edici olduğu gösterilmiştir. TRPM2 kanal proteini hücre içine fazla kalsiyum alımıyla Alzheimer patolojisini negatif etkilemektedir. Son araştırmalar kurkuminin in vitro indüklenmiş TRPM2 kanal proteinini inhibe edebildiğini rapor etmiştir. Bu çalışmanın amacı in vivo olarak Alzheimer sıçan modelinde kurkuminin TRPM2 genine ve hastalık patolojisine olan etkilerinin araştırılmasıdır. Materyal ve Metot: Araştırmada 50 adet Wistar albino cinsi erkek sıçan kullanıldı. Alzheimer model incelemesi Morris su tankı deneyiyle yapıldı. Sıçanların beyin dokusundan SOD, MDA, GSH düzeyleri spektrofotometrik yöntemlerle ölçüldü. Sıçanların hipokampus dokularından TRPM2 ve MAPT genlerinin ifadeleri gerçek zamanlı-PZR analiziyle yapıldı. Beyin dokularından hemotoksilen-eozin boyaması ile histopatolojik incelemeler yapıldı. Bulgular: STZ grubu sıçanlarda MDA seviyesi sadece kurkumin grubuna göre arttı. GSH seviyeleri STZ grubunda azalmış, STZ+kurkumin grubunda artmış olarak bulundu (P<0.05). SOD aktivitesi STZ grubunda diğer gruplara göre artmışken STZ+kurkumin grubunda bu gruba oranla azalmış gözlendi (P <0.05). TRPM2 mRNA seviyesi STZ grubunda kontrole oranla yüksek, STZ+kurkumin grubunda STZ'ye oranla azalmış bulundu. Histopatolojik olarak STZ grubu sıçan beyin dokularında nörodejenerasyon gözlendi ve kurkumin uygulamasının STZ+Kurkumin grubundadejenerasyonu hafiflettiği tespit edildi. Sonuç: STZ uygulanan sıçanlarda oksidatif stres ve nörodejenerasyon görülmüş olup ve TRPM2 gen ifadesi artırmıştır. Kurkumin uygulaması nörodejenerasyonda iyileştirme yaparken,TRPM2gen ifadesinde azalmaya yol açmıştır. Anahtar Kelimeler: Alzheimer hastalığı, kurkumin, streptozotosin, sıçan, TRPM2Öğe Investigation of the Effects of Thalidomide Against Global Cerebral Ischemia-Reperfusion Injury in Rats(Karger, 2018) Mete, Ugur Cem; Ozhan, Onural; Parlakpinar, Hakan; Yildiz, Azibe; Vardi, Nigar; Durhan, Merve; Cigremis, Yilmaz[Abstract Not Available]Öğe Investigation of the effects of thalidomide against global cerebral ıschemia-reperfusion ınjury inrats(KARGER, ALLSCHWILERSTRASSE 10, CH-4009 BASEL, SWITZERLAND, 2018) Mete, Ugur Cem; Ozhan, Onural; Parlakpinar, Hakan; Yildiz, Azibe; Vardi, Nigar; Durhan, Merve; Cigremis, Yilmaz; Kaya, Gul Busra; Acet, AhmetÖğe Neuroprotective effect of transient receptor potential Vanilloid 1 agonist capsaicin in Alzheimer?s disease model induced with okadaic acid(Elsevier, 2023) Cakir, Murat; Yuksel, Furkan; Ozkut, Mahmud Mustafa; Durhan, Merve; Kaymak, Emin; Tekin, Suat; Cigremis, YilmazBackground: The presence of Transient Receptor Potential Vanilloid 1 (TRPV1) channels was detected in many regions of the human and rat brain, including the cortex and hippocampus. TRPV1 channels have functions such as the modulation of synaptic transmission and plasticity and the regulation of cognitive functions. Previous studies conducted with TRPV1 agonists and antagonists show that this channel is associated with the neuro-degenerative process. In the present study, the purpose was to investigate the effects of capsaicin, which is a TRPV1 agonist, and capsazepine, a TRPV1 antagonist, in the Alzheimer's Disease (AD) model that was induced by intracerebroventricular (ICV) administration of okadaic acid (OKA). Methods: The AD-like experimental model was created with bilateral ICV OKA injection. Intraperitoneal capsaicin and capsazepine injections were administered to the treatment groups for 13 days and histological and immu-nohistochemical examinations were performed from the cortex and hippocampal CA3 regions of the brain. The Morris Water Maze Test was used for spatial memory measurement.Results: ICV OKA administration increased the levels of caspase-3, phosphorylated-tau-(ser396), A beta, TNF-alpha, and IL1-beta, from the cortex and hippocampal CA3 regions of the brain and decreased the phosphorylated-Glycogen synthase kinase-3 beta-(ser9) levels. In addition, the OKA administration corrupted the spatial memory. The TRPV1 agonist capsaicin reversed the pathological changes induced by ICV OKA administration, but not the TRPV1 antagonist capsazepine.Conclusions: It was found in the study that the administration of the TRPV1 agonist capsaicin reduced neuro-degeneration, neuroinflammation, and deterioration in spatial memory in the AD model induced by OKA.
