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ACA, an inhibitor phospholipases A2 and transient receptor potential melastatin-2 channels, attenuates okadaic acid induced neurodegeneration in rats
(Pergamon-Elsevier Science Ltd, 2017) Cakir, Murat; Duzova, Halil; Tekin, Suat; Taslidere, Elif; Kaya, Gul Busra; Cigremis, Yilmaz; Ozgocer, Tuba
Aim: In recent studies, it has been shown that the Transient Receptor Potential Melastatin-2 Channels (TRPM2) and Phospholipases A2 (PLA(2)) inhibitors may have a protective effect on neurons. This study was aimed to investigate the protective effect of TRPM2 and PLA(2) inhibitor N-(p-amylcinnamoyl) Anthranilic Acid (ACA) in a neurodegenerative model induced by Okadaic Acid (OKA). Main methods: OKA (200 ng/10 mu l) was administered bilateral intracerebroventricularly as a single injection. Key findings: OKA-treated rats showed significant impairments of spatial memory in Morris Water Maze Test. OKA-induced memory-impaired rats showed increased numbers of degenerated neurons and Caspase-3, tau phosphorylated ser396, beta-amyloid positive cells in the hippocampus and cerebral cortex. Furthermore, OKA-treated rats exhibited significantly increased MDA, TNF-alpha levels, and decreased SOD, GSH-PX enzyme activates and GSH levels of the tissues. ACA administration ameliorated OKA-induced memory impairment in rats. The ACA treatment also increased SOD and GSH-PX enzyme activation and GSH levels, and conversely decreased the levels of MDA, TNF-alpha. It was found that the numbers of the degenerated neurons and Caspase-3 positive cells of cortex and hippocampus regions were significantly reduced. Significance: ACA administration attenuates the oxidative stress and neuroinflammation of OKA-induced neurodegeneration; and ameliorates the cognitive decline and neurodegeneration. (C) 2017 Elsevier Inc. All rights reserved.
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, Yusuf
Acrylamide (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.
Acute and Subacute Effects of Low Versus High Doses of Standardized Panax ginseng Extract on the Heart: An Experimental Study
(Humana Press Inc, 2019) Parlakpinar, Hakan; Ozhan, Onural; Ermis, Necip; Vardi, Nigar; Cigremis, Yilmaz; Tanriverdi, Lokman H.; Colak, Cemil
Panax ginseng is commonly used in Chinese medicine and Western herbal preparations. However, it has also been recently noted to be associated with some cardiac pathologies-including cardiogenic shock due to acute anterior myocardial infarction, trans-ischemic attack, and stent thrombosis. This study was aimed to elucidate acute and subacute effects of the low and high doses of standardized Panax ginseng extract (sPGe) on cardiac functions. Rats were randomly assigned to control group, acute low-dose group (ALD), subacute low-dose group (SALD), acute high-dose group (AHD), and subacute high-dose group (SAHD). The cardiac effects of sPGe were evaluated using hemodynamic, biochemical, echocardiographic, genetic, and immunohistopathologic parameters. Mean blood pressures were significantly lower in all sPGe-treated groups compared with the control group. Troponin I and myoglobin levels were increased in the SALD, AHD, and SAHD groups. Mitral E-wave velocity was reduced after sPGe administration in all the groups. Acidophilic cytoplasm and pyknotic nucleus in myocardial fibers were observed in AHD and SAHD groups. Cu/Zn-SOD1 gene expressions were significantly higher in the sPGe-treated groups whereas caveolin 1 and VEGF-A gene expressions were not changed. According to our results, sPGe may have a potential effect to cause cardiac damage including diastolic dysfunction, heart failure with preserved ejection fraction, and reduction of blood pressure depending on the dose and duration of usage. Healthcare professionals must be aware of adverse reactions stemming from the supplementation use, particularly with cardiac symptoms.
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, Yilmaz
Aim: 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.
Amelioration of subchronic acrylamide toxicity in large intestine of rats by organic dried apricot intake
(Tubıtak scıentıfıc & technıcal research councıl turkey, ataturk bulvarı no 221, kavaklıdere, ankara, 00000, turkey, 2015) Erdemli, Mehmet Erman; Dogan, Zumrut; Cigremis, Yilmaz; Akgoz, Muslum; Altintoz, Eyup; Gecer, Murat; Turkoz, Yusuf
Acrylamide (AA) has neurotoxic, mutagenic, and genotoxic effects in humans and experimental animals. Fruit consumption is important for human health, because fruits are the source of many nutrients such as vitamins, minerals, carotenoids, dietary fiber, and phytonutrients. Many agricultural products provide natural melatonin in the diet. At the onset of the study, rats were weighted and randomly divided into four groups each containing 10 rats as follows: group 1: control (fed with normal diet and normal drinking water); group 2: apricot (fed with a daily diet with 5% apricot and normal drinking water); group 3: AA (administered daily acrylamide at 500 mu g/kg b.w. via drinking water and fed a normal diet); group 4: apricot-AA (administered daily acrylamide at 500 mu g/kg b.w. via drinking water and fed with a diet with 5% apricot). The diet schedule was continued for 12 weeks. At the end of the study, samples of large intestine were collected for biochemical analyses. The highest lipid peroxidation (as malondialdehyde, MDA) levels were observed in the AA groups, but MDA levels decreased significantly (P < 0.05) with apricot intake. Glutathione peroxidase activity in the apricot-AA group was higher than in the other three groups (P < 0.05). Glutathione S-transferase (GST) enzyme activity increased significantly in the AA group as compared with the other groups (P < 0.05). However, GST activity was significantly (P < 0.05) decreased by the apricot-supplemented diet. GST-Pi mRNA levels in the AA group increased significantly (P < 0.05) as compared with the other groups. In conclusion, the results of the current study demonstrated that AA caused large intestine damage and showed the efficiency of apricot in preventing this damage by inhibiting lipid peroxidation and improving antioxidant enzyme activities.
ASSOCIATION OF BDNF / TRKB AND NGF / TRKA LEVELS IN POSTMORTEM BRAIN WITH MAJOR DEPRESSION AND SUICIDE
(Medicinska Naklada, 2021) Erbay, Lale Gonenir; Karlidag, Rifat; Oruc, Mficahit; Cigremis, Yilmaz; Celbis, Osman
Background
Beneficial role of aminoguanidine on acute cardiomyopathy related to doxorubicin-treatment
(Springer, 2006) Cigremis, Yilmaz; Parlakpinar, Hakan; Polat, Alaadin; Colak, Cemil; Ozturk, Feral; Sahna, Engin; Ermis, Necip
Doxorubicin (DOX) is a broad-spectrum anthracycline antibiotic that has cardiotoxicity as a major side effect. One mechanism of this toxicity is believed to involve the reactive oxygen radical species (ROS); these agents likely account for the pathophysiology of DOX-induced cardiomyopathy. Aminoguanidine (AG) is an effective antioxidant and free radical scavenger which has long been known to protect against ROS formation. We investigated the effects of AG on DOX-induced changes in thiobarbituric acid reactive substances (TBARS) and reduced glutathione (GSH) content. The rats were divided into four groups:1) Control; 2) DOX group; injected intraperitoneally (i.p.) with DOX 20 mg/kg in a single dose 3) AG-treated group; injected i.p. in single dose of 20 mg/kg DOX plus 100 mg/kg AG 1 h before the DOX for 3 days, 4) AG group; injected i.p. with AG 100 mg/kg for 3 days. DOX administration to control rats increased TBARS and decreased GSH levels. AG administration before DOX injection caused significant decrease in TBARS and increase in GSH levels in the heart tissue when compared with DOX only. Morphological changes, including severe myocardial fibrosis and inflammatory cell infiltration were clearly observed in the DOX-treated heart. AG reversed the DOX-induced heart damage. Therefore AG could protect the heart tissue against free radical injury. The application of AG during cancer chemotherapy may attenuate tissue damage and improve the therapeutic index of DOX.
Cannabinoid type 2 receptor agonist JWH-133, attenuates Okadaic acid induced spatial memory impairment and neurodegeneration in rats
(Pergamon-Elsevier Science Ltd, 2019) Cakir, Murat; Tekin, Suat; Doganyigit, Zuleyha; Erden, Yavuz; Soyturk, Merve; Cigremis, Yilmaz; Sandal, Suleyman
Aim: Cannabinoid system has various physiological roles such as neurogenesis, synaptic plasticity and emotional state regulation in the body. The presence of cannabinoid type 2 receptor (CB2), a member of the cannabinoid system, was detected in different regions of the brain. CB2 receptor plays a role in neuroinflammatory and neurodegenerative processes. We aimed to determine the possible effect of CB2 agonist JWH-133 in Okadaic acid (OKA)-induced neurodegeneration model mimicking Alzheimer's Disease (AD) through tau pathology. Materials and methods: In this study, 40 Sprague Dawley male rats were divided into 4 groups (Control, Sham, OKA, OKA + JWH-133). Bilateral intracerebroventricular (icv) injection of 200 ng OKA was performed in the OKA group. In the OKA + JWH-133 group, injection of JWH-133 (0.2 mg/kg) was performed intraperitoneally for 13 days different from the group of OKA. Morris water maze test was used to evaluate the spatial memory. Levels of caspase-3, phosphorylated tau (ser396), amyloid beta (A beta), tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta) levels in brain cortex; and the hippocampus regions were examined by immunohistochemical methods. Key findings: In the OKA group, caspase-3, phosphorylated tau (ser396), A beta, IL-1 beta levels were higher in the cortex and hippocampus than in the other groups. The implementation of the JWH-133 reversed the increments in these parameters, and also prevented spatial memory impairment.
Central irisin administration suppresses thyroid hormone production but increases energy consumption in rats
(Elsevier Ireland Ltd, 2018) Tekin, Suat; Erden, Yavuz; Ozyalin, Fatma; Onalan, Ebru Etem; Cigremis, Yilmaz; Colak, Cemil; Tekedereli, Ibrahim
Irisin, which is secreted from the skeletal muscle in response to physical exercise and defined as a thermogenic peptide, may play an important role in energy metabolism. Thyroid hormones, which are one of the other influential factors on the metabolic status, increase heat production and are the main regulators of energy metabolism. This study was conducted to determine the possible effects of irisin administration on thyroid hormones. Forty adult male Wistar albino rats were used in the study. The rats were equally divided into 4 groups (n = 10). The brain infusion kit was implanted in the groups, and irisin (or solvent as control) was centrally administered to the rats via osmotic mini pumps for 7 days. During the experiment, food consumption, body weights, and body temperatures of the animals were recorded. Food intake was significantly increased in the groups treated with irisin (p < 0.05), but their body weights were not changed. Hypothalamic TRH gene expression, serum TSH, fT3, and fT4 levels were significantly lower in the groups treated with irisin as compared to the naive and control groups (p < 0.05). In addition, irisin increased UCP1 mRNA expression in white and brown adipose tissue and UCP3 mRNA expression in muscle tissue in rats and also raised their body temperature (p < 0.05). Consequently, although central irisin administration has inhibitory effects on the hypothalamic-pituitary thyroid axis, it seems to be an important agent in the regulation of food intake and energy metabolism.
Central irisin administration suppresses thyroid hormone production but increases energyconsumption in rats
(Elsevıer ıreland ltd, elsevıer house, brookvale plaza, east park shannon, co, clare, 00000, ıreland, 2018) Tekin, Suat; Erden, Yavuz; Ozyalin, Fatma; Cigremis, Yilmaz; Colak, Cemil; Tekedereli, Ibrahim; Sandal, Suleyman
Irisin, which is secreted from the skeletal muscle in response to physical exercise and defined as a thermogenic peptide, may play an important role in energy metabolism. Thyroid hormones, which are one of the other influential factors on the metabolic status, increase heat production and are the main regulators of energy metabolism. This study was conducted to determine the possible effects of irisin administration on thyroid hormones. Forty adult male Wistar albino rats were used in the study. The rats were equally divided into 4 groups (n = 10). The brain infusion kit was implanted in the groups, and irisin (or solvent as control) was centrally administered to the rats via osmotic mini pumps for 7 days. During the experiment, food consumption, body weights, and body temperatures of the animals were recorded. Food intake was significantly increased in the groups treated with irisin (p < 0.05), but their body weights were not changed. Hypothalamic TRH gene expression, serum TSH, fT3, and fT4 levels were significantly lower in the groups treated with irisin as compared to the naive and control groups (p < 0.05). In addition, irisin increased UCP1 mRNA expression in white and brown adipose tissue and UCP3 mRNA expression in muscle tissue in rats and also raised their body temperature (p < 0.05). Consequently, although central irisin administration has inhibitory effects on the hypothalamic-pituitary thyroid axis, it seems to be an important agent in the regulation of food intake and energy metabolism.
Comparative Analysis of Human and Porcupine (Hystrix Cristata L., 1758) Haemoglobins
(Gazi Univ, 2008) Cigremis, Yilmaz; Atalar, Omer; Erdogan, Kenan; Gaffaroglu, Muhammet; Turkoz, Yusuf; Yilmaz, Sadik
Agarose gel electrophoresis was used to determine the electrophoretic pattern of the haemoglobin of Hystrix cristata (H. cristata), and that of a healthy human. Alkaline agarose gel electrophoresis of the haemoglobin of H. cristata revealed that the mobility of the H. cristata haemoglobin was considerably faster than that of human haemoglobin. These comparisons showed obvious differences between the haemoglobin of the two species.
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, Yusuf
Background: 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.
Cucurbitacin I exhibits anticancer efficacy through induction of apoptosis and modulation of JAK/STAT3, MAPK/ERK, and AKT/mTOR signaling pathways in HepG2 cell line
(Wiley-Hindawi, 2022) Uremis, Nuray; Uremis, Muhammed Mehdi; Cigremis, Yilmaz; Tosun, Emir; Baysar, Ahmet; Turkoz, Yusuf
Hepatocellular carcinoma is a common cancer type, especially among men. Although cucurbitacin I (CuI), widely found in plants belonging to the Ecballium elaterium (E. L) plant family, has been shown to have antitumorigenic properties in many cancer types, its anticancer effect, molecular mechanism, and apoptotic effect mediated by signal pathways on hepatocellular carcinoma have not been fully clarified. In the present study, we investigated the anticancer effect of CuI treated at different doses on the HepG2 cell line and the underlying mechanism in vitro. High-purity CuI was obtained from the E. elaterium plant with the aid of HPLC. The effects of this substance on the viability of cells were studied by the MTT assay. The effects of CuI on cell cycle progression and apoptosis were studied with flow cytometry. DNA breaks were analyzed by the Comet assay method. The proteins and genes involved in the JAK/STAT3, MAPK/ERK, and AKT/mTOR signaling pathways were investigated using Western blot and qRT-PCR, respectively. The results of this study demonstrated that CuI significantly reduced HepG2 cell growth in vitro, induced antiproliferation, and G2/M phase of the cell cycle was interrupted. Practical applications CuI administration was shown to downregulate the levels of proteins in the PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 cascades in HepG2 cells. CuI also reduced the expression of MAPK, STAT3, mTOR, JAK2, and Akt genes in different concentrations. DNA breaks are formed as a result of this effect. CuI, by reducing cell proliferation and promoting apoptosis, was found to have potential as a chemotherapeutic agent of hepatocellular carcinoma.
Dose-dependent subacute cardiovascular effects of modafinil in rats
(Taylor & Francis Ltd, 2022) Canyurt, Dilan; Tanriverdi, Lokman Hekim; Ozhan, Onural; Cansel, Mehmet; Parlakpinar, Hakan; Vardi, Nigar; Cigremis, Yilmaz
Modafinil is used for the treatment of various sleep disorders; however, its usage among healthy individuals is also increasing. There are a limited number of cardiovascular side effects, including ischemic T-wave changes, dyspnea, hypertension, and tachycardia in the literature. Our research aimed to investigate the dose-dependent subacute cardiovascular effects of modafinil in rats. Thirty-two rats were randomly and equally assigned to a control group (vehicle-treated for 14 days), a subacute low-dose group (SALD, 10 mg/kg for 14 days), a subacute moderate-dose group (SAMD, 100 mg/kg for 14 days), and a subacute high-dose group (SHD, 600 mg/kg for 14 days). The cardiovascular effects of modafinil were evaluated using hemodynamic, biochemical, electrocardiographic, electrophysiologic, and histopathologic parameters. In terms of hemodynamic parameters, heart rate, and systolic/diastolic/mean blood pressure levels, electrophysiological parameters did not reach statistical significance among the groups (p > 0.05). The incidence of T-wave negativity in SAMD and SAHD groups was 25 and 37.5%, respectively. Moreover, one rat per group was affected by an atrioventricular blockage. Malondialdehyde, superoxide dismutase, catalase, and reduced glutathione levels in the heart and vascular tissues, serum troponin-I, and creatine kinase levels were similar between the modafinil-administered groups and the control group (p > 0.05); this indicates that modafinil activated neither oxidative stress nor antioxidant pathway. Also, there was no difference in histopathological parameters between groups (p > 0.05). Supratherapeutic doses of modafinil may have the potential to cause ischemic cardiac damage and atrioventricular blockage, despite inconsistency with literature findings; however, this does not pertain to hemodynamic changes.
The effect of apocynin on motor and cognitive functions in experimental Alzheimer's disease
(Periodicum Biologorum, 2018) Akyuva, Yener; Onal, Cagatay; Parlakpinar, Hakan; Gul, Mehmet; Cigremis, Yilmaz; Ates, Tuncay; Kablan, Yuksel
Scope: We investigated the potential beneficial effect of Apognin (APO) on motor and cognitive functions in experimental Alzheimer's disease (AD). Materials and Methods: Experimental AD was induced in rats by intraventricular streptozotocin (STZ) injection. Sham group received articial cerebrospinal fiuid (CSF). Both groups were randomly divided into two subgroups. One of the subgroups received intraperitoneal APO for while the other had normal saline (NS). The animals were evaluated with rotarod, accelerod and Water-Maze tests before and after the treatment. Additionally, biochemical markers of oxidative stress such as malondialdehyde (MDA) and reduced glutathione (GSH) were analyzed fiom brain specimens. Standard histological evaluation and transmission electron microscopy (TEM) were used to evaluate the neural damage. Results: The difference between S7Z+NS in comparison with CSF+NS, CSF+APO and STZ+APO were statistically significant on 30 and 40 rpm on rotarod test. GSH levels, accelerod and Water-Maze test results were not statistically significant between subgroups. However, MDA differences between STZ+NS in comparison with CSF+NS, CSF+APO and STZ+APO were statistically significant. Hemotoxikne eozine staining and TEM results showed apocynins protective effect. Conclusion: These results indicate that APO can provide neuro-protective effect for motor but not for cognitive performance in experimental AD.
The effect of apricots on the experimental cataract model formed by sodium selenite
(Pergamon-Elsevier Science Ltd, 2013) Doganay, Selim; Duz, Cem; Firat, Penpe Gul; Cankaya, Cem; Kutukde, Derya; Cigremis, Yilmaz
This study was designed in order to investigate whether sun dried apricots have a preventive effect on the experimental cataract model formed by sodium selenite in rats. Fifty-nine Spraque-Dawley rat pups were divided into three groups. Group I (control group) consisted of twenty rat pups, born from the rats nourished ad libitum. Group 2 consisted of 18 newborn rats, born from the rats nourished ad libitum with 10% sun dried natural apricots. Group 3 consisted of 21 newborn rats, born from the rats nourished ad libitum. Subcutaneous (30 nmol/gr) sodium selenite injection was applied to all the newborn rats except the control group (Group 1) on postpartum day 10. Cataract development was graded by slit-lamp examination and photography. Encapsulated lenses were analyzed for reduced glutathione (GSH) and malondialdehyde (MDA), a marker of lipid per oxidation. Lenses were also analyzed for total nitrite (TN). The presence of oxidative stress in selenite cataract development and its prevention by sun dried apricots. (C) 2013 Elsevier Ltd. All rights reserved.
Effect of Cannabinoid Type 2 Receptor Activation in Okadaic Acid Induced Rat Alzheimer's Disease Model
(Wiley, 2018) Cakir, Murat; Doganyigit, Zuleyha; Tekin, Suat; Erden, Yavuz; Cigremis, Yilmaz; Sandal, Suleyman
[Abstract Not Available]
Effect of cannabinoid type 2 receptor activation in okadaic acid ınduced rat alzheimer's disease model
(Acta physıologıca, 2018) Çakır, Murat; Doğanyiğit, Züleyha; Tekin, Suat; Erden, Yavuz; Cigremis, Yilmaz; Sandal, Suleyman
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]
Effect of Intracerebroventricular Administration of Apelin-13 on the Hypothalamus-Pituitary-Thyroid Axis and Peripheral Uncoupling Proteins
(Springer, 2018) Erden, Yavuz; Tekin, Suat; Tekin, Cigdem; Ozyalin, Fatma; Yilmaz, Umit; Onalan, Ebru Etem; Cigremis, Yilmaz
Apelin, a ligand for G protein-coupled APJ receptor, is a peptide hormone. Although apelin and APJ receptors are determined in hypothalamus and thyroid gland its role in the hypothalamus-pituitary-thyroid (HPT) axis and mechanism of action on energy metabolism is not clear. This suggests that apelin may play a role in the HPT axis and energy metabolism. This study was designed to determine possible effects of centrally administered apelin-13 on the HPT axis and energy metabolism. A total of 40 adult male Sprague Dawley rats were divided into four groups (n=10 each group). Intact rats served as control group while the sham group received vehicle of apelin. Apelin-13 was injected intracerebroventricularly at the doses of 1 and 10nmol, for 7 days in the rats in the experimental group. At the end of the experimental protocol, animals were decapitated and brain, blood, white and brown adipose tissues samples were collected. There was no significant difference between the groups in terms of hypothalamic TRH mRNA levels. Serum TSH levels were significantly higher in all groups compared to the control group (p<0.05). Serum fT3 and fT4 levels were significantly lower in apelin-13 administered groups (p<0.05). Moreover, apelin-13 administered groups had lower levels of UCP1 mRNA in white and brown adipose tissues. UCP3 mRNA expression in muscle tissue was also lower in apelin-13 treated groups (p<0.05). These results indicates that apelin-13 exhibits a decreasing effect on energy consumption through a mechanism involving the peripheral rather than central arms of the HPT axis.

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