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- ArticleAçık Erişim2026The Relationship Between Non-alcoholic Fatty Liver Disease and Epicardial Adipose Tissue Thickness, Carotid Intima Media Thickness, and Aortic Propagation Velocity
Aydin, Sonay; Ozcicek, Fatih; Hayme, Serhat; Coşgun, Muharrem Said; Ozturk, Ersin; Öztürk, Gülay Kızılgün
Objective: Cardiovascular disease is prevalent among individuals diagnosed with non-alcoholic fatty liver disease (NAFLD). Epicardial adipose tissue (EAT), carotid intima-media thickness (CIMT), and aortic propagation velocity (APV) are associated with atherosclerosis and cardiovascular disease (CVD). The aim of this study is to determine whether NAFLD is associated with EAT, CIMT, and APV. Methods: Individuals aged ≥18 and <65 years who presented for routine follow-up were included. The study population comprised 75 healthy controls (40 females, 35 males) and 141 patients with NAFLD (68 females, 73 males). Epicardial adipose tissue thickness, carotid intima-media thickness, and aortic propagation velocity were evaluated using transthoracic echocardiography in patients who were diagnosed with hepatosteatosis by ultrasound during routine check-ups at the internal medicine clinic. Results: NAFLD was positively associated with epicardial adipose tissue thickness and carotid intima–media thickness, and negatively associated with aortic propagation velocity. Patients with NAFLD had significantly higher EAT and CIMT values and lower APV values than controls. Logistic regression analysis identified body mass index (BMI) and EAT as independent predictors of hepatosteatosis. Each unit increase in BMI was associated with a 1.29-fold increase in the risk of hepatosteatosis, whereas each unit increase in EAT was associated with a 5.49-fold increase. Conclusion: Given the established associations of CIMT, APV, and EAT with atherosclerosis and cardiovascular disease, assessment of patients with NAFLD using these noninvasive parameters may help identify subclinical cardiovascular risk.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2025The relationship between rheumatoid arthritis and epicardial fat thickness, and serum levels of chemerin, adropin, and betatrophin
Ekinci, Bilge; Mertoglu, Cuma; Coskun, Resit; Arslan, Yusuf Kemal; Coban, Taha Abdulkadir; Ozcicek, Fatih
Background. Cardiovascular diseases (CVDs) are highly prevalent among patients with rheumatoid arthritis (RA). Epicardial adipose tissue, serum betatrophin, chemerin, and adropin levels are factors associated with atherosclerosis and cardiovascular involvement. Objectives. This study aimed to investigate the relationship between RA and epicardial fat thickness (EFT), as well as serum betatrophin, chemerin and adropin levels. Materials and methods. This cross-sectional study included 80 patients (62 women and 18 men) diagnosed with RA according to the American College of Rheumatology/The European Alliance of Associations for Rheumatology (ACR/EULAR) 2010 RA classification criteria and 80 healthy controls (64 women and 16 men). Exclusion criteria comprised other autoimmune diseases, CVDs, diabetes mellitus, other endocrine disorders, acute or chronic pancreatic disorders, malignancy, pregnancy, breastfeeding, or antihyperlipidemic drug usage. Serum betatrophin, chemerin and adropin concentrations were measured. Epicardial fat thickness was evaluated with transthoracic echocardiography. Results. Adropin levels were significantly lower in the RA group compared to the control group (p < 0.001). Chemerin levels and EFT were significantly higher in the RA group than in the control group (p = 0.016, p < 0.001, respectively). When assessing the relationship between biomarkers and EFT in RA patients, a strong positive correlation was observed between chemerin and EFT (r = 0.73, p = 0.046) in patients with high disease activity. Conclusions. Epicardial fat thickness, as an indicator of cardiovascular involvement, is higher in patients with RA. Moreover, high chemerin levels and low adropin levels in these patients may be indicative of cardiovascular involvement. Copyright by Author(s)
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023Effect of Thiamine Pyrophosphate upon Possible Metamizole-Induced Liver Injury in Rats
Bedir, Zehra; Erdem, Kezban Tuna Ozkaloglu; Can, Abdullah; Cicek, Betul; Gulaboglu, Mine; Suleyman, Zeynep; Gursul, Cebrail; Mokhtare, Behzad; Ozcicek, Fatih; Suleyman, Halis
Background and Objective: Metamizole is a non-selective cyclooxygenase (COX) inhibitor NSAID with a strong analgesic and spasmolytic effects. It is the most common analgesic in the world. Thiamine pyrophosphate (TPP) protects the liver tissue against oxidative damage. The aim of our study was to analyze the effect of TPP against possible liver injury and dysfunction of metamizole in rats biochemically and histopathologically. Materials and Methods: The animals were grouped as healthy (HG), 500 mg kg(-1) metamizole (MT-500), 1000 mg kgG1 metamizole (MT-1000), 25 mg kg(-1) TPP+500 mg kg(-1) metamizole (TMT-500), 25 mg kg(-1) TPP+1000 mg kg(-1) metamizole (TMT-1000) groups. The TMT-500 and TMT-1000 groups of animals were injected intraperitoneally (ip) at the dose of 25 mg kg(-1) of TPP. Distilled water as the solvent was injected ip to the HG, MT-500 and MT-100 groups. One hour after injecting TPP and distilled water, metamizole 500 and 1000 mg kg(-1) doses were administered orally to the TMT-500 and TMT-1000 groups. The TPP was administered once and metamizole twice a day for 14 days. The animals were euthanized with high-dose anesthesia. The liver tissues excised from the animals were analyzed biochemically and histopathologically. Results: In both doses metamizole significantly increased MDA, ALT and AST levels and decreased tGSH, SOD and CAT levels compared to the healthy group. TPP significantly prevented the decrease of tGSH, SOD and CAT levels and the increase of MDA, ALT and AST levels with metamizole. There was no statistical difference in all of the levels between the TMT-500 and TMT-1000 groups. The histopathological findings indicated TPP significantly suppressed the damage induced by metamizole. Conclusion: The metamizole was possible to cause moderate damage to liver tissue. Therefore, it was considered that the use of TTP to reduce liver toxicity could be clinically beneficial.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Effect of Liv-52 on Atorvastatin Induced Hepatotoxicity in Rats: A Biochemical and Histopathologic Study
Icel, Aykut; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Cicek, Betul; Yazici, Gulce Naz; Gulaboglu, Mine; Ozcicek, Fatih; Suleyman, Halis
Background and Objective: The toxic effect of atorvastatin on the liver has been associated with oxidative stress. The Liv-52 is a polyherbal formulation with known hepatoprotective properties. In this study, the preventive effect of Liv-52 against the potential hepatotoxicity of atorvastatin was investigated. Materials and Methods: Eighteen rats were categorized into three groups of six rats each: Healthy group (HG), atorvastatin-treated group (ATC) and Liv-52+atorvastatin-treated group (LAT). The Liv-52 was orally administered at 50 mg kg(-1) and atorvastatin was orally given at 20 mg kg(-1) after 1 hr of Liv-52 administration. The Liv-52 and atorvastatin were administered once daily for two months. At the end of two months, blood samples were collected from the rats. Subsequently, rats were sacrificed under high-dose (50 mg kg(-1)) thiopental anesthesia and liver tissues were extracted. Biochemical analysis of extracted liver tissues and serum was performed. Liver tissues were additionally analyzed for histopathology. Results: The Liv-52+atorvastatin administration inhibited the atorvastatin-induced increase in malondialdehyde and decreased total glutathione and superoxide dismutase activities in the liver tissues. In addition, the rats receiving Liv-52 had lower levels of serum alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase compared to the atorvastatin group. Histopathologic analysis demonstrated that Liv-52 protected the liver tissue against atorvastatin-induced injury. Conclusion: The Liv-52 therapy may be useful in preventing atorvastatin-induced liver injury.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Effects of taxifolin on aspirin-induced gastric damage in rats: macroscopic and biochemical evaluation
Cerrah, Serkan; Akbas, Nergis; Ozcicek, Fatih; Mammadov, Renad; Altuner, Durdu; Suleyman, Halis; Bulut, Seval
Taxifolin (dihydroquercetin) is a flavanonol isolated from various plants and has antioxidant effects. The aim of our study was to macroscopically and biochemically investigate the effects of taxifolin on aspirin-induced oxidative gastric damage in rats and to evaluate them by comparison with those of famotidine. Rats were divided into four drug administration groups: a healthy control group, an aspirin-only group (ASG), a taxifolin + aspirin group (TASG), and a famotidine + aspirin group (FASG). The results revealed that in light of the results that we obtained, 50 mg/kg taxifolin had anti-ulcer effects. At this dose, taxifolin was able to bring COX-1 activities to a level close to those seen in healthy rats with appropriate macroscopic, oxidant/antioxidant, and biochemical parameters. Based on these results, it can be said that taxifolin may be successfully used as a more potent alternative to famotidine, which is the currently accepted treatment for aspirin-induced ulcers.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Carvacrol prevents acrylamide-induced oxidative and inflammatory liver damage and dysfunction in rats
Cerrah, Serkan; Ozcicek, Fatih; Gundogdu, Betul; Cicek, Betul; Coban, Taha Abdulkadir; Suleyman, Bahadir; Altuner, Durdu; Bulut, Seval; Suleyman, Halis
Background: Acrylamide causes hepatotoxicity with the effect of oxidative stress and inflammatory processes. Carvacrol is a monoterpenic phenol with antioxidant and anti-inflammatory properties. Aims: To determine the effects of carvacrol on oxidative liver injury induced by acrylamide administration in rats. Methods: Rats were divided into three groups of six animals each: healthy group acrylamide group (ACR), and acrylamide + carvacrol group (TACR). First, carvacrol (50 mg/kg) was administered intraperitoneally to the CACR group. One hour later, acrylamide (20 mg/kg) was given orally to the ACR and CACR groups. This procedure was performed for 30 days, after which the animals were sacrificed. The malondialdehyde (MDA) and total glutathione (tGSH) levels, total oxidant (TOS) and total antioxidant status (TAS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and nuclear factor kappa b (NF-κB) were measured in the excised liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were determined in blood serum samples. Liver tissues were also examined histopathologically. Results: In the ACR group, malondialdehyde, TOS, ALT, AST levels, and NF-κB, IL-1β, and TNF-α levels were found to be high, and tGSH and total antioxidant status levels were low. In addition, diffuse degenerative changes and necrosis in hepatocytes, and moderate inflammation in the portal region were detected in the liver tissues of the ACR group. While carvacrol prevented the biochemical changes induced by acrylamide, it also alleviated the damage in the histological structure. Conclusion: Carvacrol may be used for liver damage caused by acrylamide.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2023The relationship between serum free testosterone level and body composition in geriatric and non-geriatric male hemodialysis patients
Kara, Ali Veysel; Doğan, Mehmet; Olmez, Hasan; Tunc, Yesim; Ozcicek, Fatih; Akbas, Emin Murat
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Evaluation of epicardial adipose tissue thickness and inflammatory parameters in smokers and non-smokers
Arslan, Yusuf Kemal; Mertoglu, Cuma; Ozcicek, Adalet; Ozcicek, Fatih; Soylu, Yasin Emrah; Çoşkun, Reşit
Smoking is the leading cause of preventable death. Epicardial adipose tissue (EAT) surrounds the heart surface and creates local and systemic effects secreting the hormones, cytokines, inflammatory mediators. Previous studies demonstrated that both smoking and EAT have a strong association with inflammation and atherosclerosis.Our study aimed to determine the relationship of smoking with EAT thickness and inflammation by evaluating smokers and non-smokers. A total of 259 healthy male and female participants between the ages of 18-65, without a history of chronic disease and with a body mass index within normal limits, were included in a study. EAT thickness measurements were made by transthoracic echocardiography and EAT thicknesses of smokers and non-smokers were compared. In addition, the effects of smoking and EAT thickness on different inflammatory parameters were evaluated. When the EAT thicknesses were compared between smokers and non-smokers (2.60±1.2), a statistically significant difference was found in favor of smokers (3.84±1.84) (p<0.001). A moderate positive correlation was found among age, body mass index, smoking duration in years, pack/year and EAT thickness. The difference among waist circumference, the number of cigarettes smoked daily, diastolic blood pressure, fasting blood glucose, ALT, AST, total cholesterol, triglyceride, LDL-cholesterol, CRP, uric acid, platelet count, MPV values, platelet/lymphocyte ratio and EAT thickness were found meaningful, but the weak correlation in different ratios were determined. Smoking was found to be the most important determinant of EAT thickness. Other determinants of EAT thickness were age, body mass index, CRP and female gender. The significant statistical relationship between smoking and EAT thickness suggests that smoking increases EAT thickness and inflammatory parameters. Co-assessment of the EAT and blood inflammatory parameters in smokers may guide the initiation of medical treatment in primary prevention or other therapies.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Effects of Mirtazapine on Liver Ischemia-Reperfusion Injury in Rats
Alemdar, Ali; Yilmaz, Ismayil; Ozcicek, Fatih; Bulut, Seval; Eden, Arif Onur; Gursul, Cebrail; Mendi, Ali Sefa; Kuzucu, Mehmet; Altuner, Durdu; Suleyman, Halis
Background and Objective: Ischemia-reperfusion (I/R) injury begins with tissue oxygen deprivation and continues with oxidative stress and inflammatory response. Mirtazapine is an antidepressant drug with antioxidant and anti-inflammatory properties. The current study was to investigate the effect of mirtazapine against I/R induced liver injury in rats. Materials and Methods: Albino Wistar-type male rats were divided into sham operation (SHAM), I/R (IR) and I/R+mirtazapine administrated (IRM) groups. One hour before anaesthesia, 20 mg kg(-1) mirtazapine was administered to the IRM group of the animals and distilled water was applied to the SHAM and IR groups as a solvent. I/R was achieved by clamping the hepatic artery (except for the SHAM group). Following I/R, all rat groups were killed with high-dose anaesthesia. Malondialdehyde (MDA), total glutathione (tGSH), nuclear factor kappa B (NF-kappa B), interleukin 1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) were determined in liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were measured in blood serum. In addition, histopathological examination was performed on liver tissue samples. Results: Mirtazapine prevented increased levels of MDA, NF-kappa B, IL-1 beta, TNF-alpha, ALT and AST in liver tissue with I/R and a decrease in tGSH. Furthermore, mirtazapine has alleviated I/R-associated severe hepatocyte degeneration, necrosis and other structural disorders in the liver. Conclusion: Biochemical and histopathological experimental results suggest that mirtazapine may be useful in the treatment of I/R-induced liver injury.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Effect of Rhodiola rosea Root Extract on Stress-Induced Gastric Ulcer in Rats
Isik, Bahar; Altuner, Durdu; Ozcicek, Fatih; Ezmeci, Talat; Aggul, Ahmet G.; Suleyman, Bahadir; Bulut, Seval; Suleyman, Zeynep; Yavuzer, Bulent; Suleyman, Halis
Stress can lead to stomach ulcers. Oxidative stress and inflammation are involved in the pathogenesis of stress ulcers. Rhodiola rosea root extract (RRE) has antistress, anxiolytic, antioxidant and anti-inflammatory effects. In this study, the effect of RRE on gastric ulcers induced by forced immobilization method (FIM) was investigated. Albino Wistar male rats were divided into healthy (HG), control (SC), stress+RRE (SRE) and stress+famotidine (SFM) groups. RRE was given to the rats’ SRE group, and famotidine to the SFM group was administered orally. One hour after, the animals in the SRE, SFM and SC groups were subjected to stress with FIM for one hour once a day. This procedure continued for seven days. After this period, the animals were euthanized. Stomach tissues were examined macroscopically and biochemically. RRE reduced the number and area of stress-induced ulcers and biochemical changes in the gastric tissues of animals better than famotidine.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Amelioration of oxidative damage parameters by carvacrol on methanol-induced liver injury in rats
Gursul, Cebrail; Ozcicek, Adalet; Ozkaraca, Mustafa; Mendil, Ali Sefa; Coban, Taha Abdulkadir; Arslan, Aynur; Ozcicek, Fatih; Suleyman, Halis
The methanol metabolite that causes hepatotoxicity is formic acid, generating reactive oxygen radical formation and cell damage. Carvacrol is an antioxidant monoterpenic phenol produced from Thymus vulgaris. This study aimed to investigate the effects of carvacrol on methanol-induced oxidative liver damage in rats. Eighteen rats were divided into three groups. Methotrexate was administered orally for 7 days to methotrexate+methanol (MTM) and methotrexate+methanol+carvacrol (MMC) groups. Methotrexate was given before methanol to cause methanol poisoning. Distilled water was given to the healthy group (HG) as a solvent. At the end of the 7th day, 20% methanol was administered orally at a dose of 3 g/kg to the MTM and MMC groups. Four hours after methanol administration, 50 mg/kg carvacrol was injected intraperitoneally into the MMC group. Animals were sacrificed 8 h after carvacrol injection. Biochemical markers were studied in the excised liver tissue and blood serum samples, and histopathological evaluations were made. Severe hemorrhage, hydropic degeneration, pycnosis, and mononuclear cell infiltration were observed in the liver of the MTM group. Additionally, the levels of malondialdehyde (MDA), total oxidant status (TOS), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were significantly higher, and total glutathione (tGSH) and total antioxidant status (TAS) were significantly lower in the MTM group compared to HG (P<0.001). Carvacrol prevented the increase in MDA, TOS, ALT and AST levels with methanol and the decrease in tGSH and TAS levels (P<0.001), and alleviated the histopathological damage. Carvacrol may be useful in the treatment of methanol-induced liver damage.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Ameliorative effects of Liv-52 on doxorubicin-induced oxidative damage in rat liver
Yildirim, Nilgun; Lale, Azmi; Yazıcı, Gulce Naz; Sunar, Mukadder; Aktas, Mehmet; Ozcicek, Adelet; Suleyman, Bahadır; Ozcicek, Fatih; Suleyman, Halis
Hepatotoxicity is a common side effect of doxorubicin (Dox) treatment of cancer. Liv-52 is an ayurvedic medicine that is reported to ameliorate liver injury due to oxidative stress. We investigated the effects of Liv-52 on Dox induced oxidative damage to liver tissues of rats using biochemical and histopathological techniques. Thirty male rats were assigned randomly into three equal groups: control (CG), Dox group (DG) Liv-52 + Dox group (LD). Rats in the LD group received 50 mg/kg Liv-52 in distilled water via gastric gavage. Distilled water was given via the same route to the rats in the DG and CG groups. Rats in the LD and DG groups were injected intraperitoneally with 5 mg/kg Dox 1 h after administration of Liv-52 or distilled water. The procedure was repeated daily for 7 days. On day 8, the animals were sacrificed, and serum and tissue biochemical and histopathological assays were performed. The malondialdehyde level was increased significantly in the DG group, while glutathione and superoxide dismutase levels were significantly lower in the DG group compared to the LD and CG groups. The highest levels of alanine aminotransferase, aspartate aminotransferase and lactate dehydrogenase were found in the DG group, while the lowest levels were found in the CG group, which exhibited levels similar to those of the LD group. Treatment with Liv-52 prior to Dox treatment reduced the histopathologic changes in the Dox group. Therefore, pre-treatment with Liv-52 protected against Dox induced oxidative stress and hepatotoxicity.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Effect of taxifolin on acrylamide-induced oxidative and proinflammatory lung injury in rats: Biochemical and histopathological studies
Demir, Omer Faruk; Elma, Bekir; Suleyman, Bahadir; Ozkaraca, Mustafa; Mammadov, Renad; Suleyman, Halis; Coban, Taha Abdulkadir; Ozcicek, Fatih
Purpose: To examine the probable beneficial effects of taxifolin against acrylamide damage in lung tissue. Methods: 18 male albino Wistar rats were divided into healthy (HG), acrylamide (AG) and taxifolin + acrylamide (TAG) groups. Once a day for 30 days, acrylamide was orally administered to the AG group (50 mg/kg), while ACL (50 mg/kg) and TAX (20 mg/kg) were orally administered to TAG group. Protein concentration, malondialdehyde (MDA), and total glutathione (tGSH) levels as well as oxidant and antioxidant molecules concentrations of the rat lung tissues were measured. In addition, degree of mononuclear (MN) cell infiltration and bronchial-associated lymphoid tissue (BALT) hyperplasia was evaluated by the degree of hyperplasia (absent, mild, moderate, severe). The histopathological and biochemical data the groups were compared. Results: When compared in terms of MDA levels, it was found that the AG group had high MDA levels, and the TAG group had low MDA levels. (p < 0.001). TAG group was found to have a higher tGSH level than the AG group (p < 0.001). Compared to the AG group, lower TOS and higher TAS levels were obtained in the TAG group (p < 0.001). In addition, when TOS levels of TAG and HG groups were compared, the TOS levels between the two groups were statistically insignificant (p = 0.213). It has been observed that TAX administration prevents the increase in NF-ƘB level. When the NF-ƘB levels of the AG and TAG groups were compared with each other, there was a statistically significant difference (p = 0.001). In the AG group, severe MN cell hyperplasia and BALT hyperplasia were observed histopathologically. It was determined that these findings were alleviated in the TAG group. A histopathologically significant difference was found between AG and TAG groups (p < 0.05). Conclusion: Taxifolin has beneficial effects against lung injury caused by acrylamide, a health-damaging environmental factor. Regular use of taxifolin can be recommended, especially in people who are known to have intense contact with acrylamide. There is a need for research studies on this subject.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Everolimus-Induced Oral Mucositis Can be Prevented by Hippophae Rhamnoides Extract in Rats
Gezer, Arzu; Cil, Ibrahim; Suleyman, Bahadir; Ozcicek, Fatih; Semiz, Huseyin Salih; Akagunduz, Baran; Ozer, Muhammet; Demircan, Nazım Can; Aktas, Mehmet; Suleyman, Halis
Objectives: Oral mucositis is a significant toxicity related to the mammalian target of rapamycin inhibitor everolimus. Oxidative stress and pro-inflammatory cytokines, which contribute to treatment-related mucositis, can betargeted with Hippophae rhamnoides extract (HRE). Herein, we assessed the effects of HRE on everolimus-inducedmucositis in rats.Methods: Eighteen rats were equally divided into healthy, everolimus, and everolimus plus HRE groups. Malondialdehyde (MDA) and total glutathione (tGSH) levels along with interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha(TNF-α) gene expression levels were measured in the tongue and buccal mucosa tissues of all groups, histopathologicalchanges were also evaluated. We tested the significance of variations with one-way variance analysis. We also analyzedthe differences between groups with Kruskal–Wallis test and Mann–Whitney U-test.Results: HRE significantly decreased MDA and increased tGSH levels and reduced IL-1β and TNF-α gene expression inboth tissues administered everolimus (p<0.001 for each). Histological examination revealed that HRE improved epithelial formation and keratinization, disrupted by everolimus, and alleviated everolimus-related mononuclear cell infiltration (p<0.05 for each).Conclusion: In light of these results, HRE may be a promising agent to manage oral mucositis caused by everolimus,given the lack of effective therapeutic options for this type of adverse event.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Molecular Mechanism of the Protective Effect of Tianeptine Against Ketamine-Induced Cardiac Injury in Rats
Yildiz, Sevler; Ugur, Kerim; Tas, Hakan G.; Ozcicek, Fatih; Kuyrukluyildiz, Ufuk; Mendil, Ali S.; Cankaya, Murat; Mamedov, Renad; Suleyman, Halis
Ketamine is a short-acting anesthetic drug that is derived from phencyclidine. Ketamine is used to treat depression and chronic pain disorders, as well as for anesthesia, analgesia, and sedation. Ketamine’s sympathomimetic characteristic causes cardiotoxicity. The pathophysiology of ketamine’s harmful impact has been linked to reactive oxygen species (ROS) and proinflammatory cytokines such as interleukin 1 beta (IL-1), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α). Tianeptine is an antidepressant that works similarly to tricyclic antidepressants. According to studies, tianeptine reduces the production of proinflammatory cytokines such as ROS, IL-1, IL-6, and TNF-α. Tianeptine has a sympatholytic action as well. All of this evidence suggests that tianeptine might help to reduce ketamine cardiotoxicity. The goal of our research is to use biochemical and histological techniques to see how tianeptine affects ketamine-induced cardiotoxicity in rats.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2020Effects of anakinra on the small intestine mucositis induced by methotrexate in rats
Ozcicek, Fatih; Kara, Ali Veysel; Akbas, Emin Murat; Kurt, Nezahat; Yazici, Gulce Naz; Cankaya, Murat; Mammadov, Renad; Ozcicek, Adalet; Suleyman, Halis
Intestinal mucositis is an important problem in the patients receiving cancer treatment. We aimed to investigate the effect of anakinra, which is a well known anti-oxidant and anti-inflammatory agent, on methotrexate-induced small intestine mucositis in rats. Forty rats were divided into 4 groups with 10 in each group. The healthy group (HG) and the methotrexate group (MTXG) were given distilled water, while the methotrexate + anakinra 50 (MTX+ANA50) and the methotrexate + anakinra 100 (MTX+ANA100) groups were intraperitoneally administered 50 and 100 mg/kg of anakinra. After one hour, the MTXG, MTX+ANA50 and MTX+ANA100 groups were given oral methotrexate at a dose of 5 mg/kg. This procedure was repeated once a day for 7 days. After the rats had been sacrificed, the small intestine tissue of rats were removed for the assesment of biochemical markers, histopathological evaluation and gene expression analyze. Statistical analyses of the data were performed using one-way ANOVA. Malondialdehyde (MDA), myeloperoxidase (MPO) and interleukin-6 (IL-6) levels were significantly higher, whereas total glutathione (tGSH) levels were significantly lower in MTXG (P<0.001) compared to other groups. MTX also increased IL-1β and TNF-α gene expression levels in MTXG (P<0.001). Inflammatory cell infiltration and damage to the villus were observed histopathologically in the MTXG group, whereas only mild inflammation was seen in the MTX+ANA100 group. A dose of 100 mg/kg of anakinra prevented the increase of the biochemical markers and gene expression levels better than a dose of 50 mg/kg. Intestinal mucositis caused by MTX may be preventible by co-administered anakinra.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2020Effects of adenosine triphosphate on vandetanib induced skin damage in rats
Akagunduz, Baran; Ozcicek, Fatih; Kara, Ali Veysel; Guven, Deniz Can; Yazici, Gulce Naz; Çoban, Abdulkadir; Suleyman, Bahadır; Mammadov, Renad; Suleyman, Halis
Purpose: Vandetanib is a wide spectrum tyrosine kinase inhibitor used for the treatment of metastatic medullary thyroid cancer (MTC) and various other cancer types. Although it is usually well-tolerated ıt has been linked to a variety of severe dermatologic reactions. Our study aimed was to investigate adenosine 5′-triphosphate (ATP) on vandetanib-induced skin damage. Materials and methods: A total number of 18 rats were divided into three equal groups as vandetanib group (VDB), vandetanib plus ATP group (VAT), and healthy group (HG); 25 mg/kg ATP was injected intraperitoneally (ip) to the VAT group. Normal saline was given to the HG and VDB groups as solvent via intraperitoneally. One hour later, 25 mg/kg vandetanib was applied orally via an orogastric catheter in the VAT and VDB groups. This procedure was repeated once daily for 4 weeks. After that period, all animals were sacrificed and their skin tissues removed. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS), total antioxidant status (TAS) levels in rats’ skin tissues were evaluated with histopathological analyses. Results: MDA and TOS levels measured higher in the VDB group compared to the VAT and HG groups (p < 0.001). tGSH and TAS levels of the VDB group measured lower than the VAT and HG groups (p < 0.001). The structure and morphology of skin tissue were normal in the control group. In the VDB group, skin tissue damage with thinner epitelium, ruptured and degenerated hair follicles, abnormal accumulation of abnormal keratin on the epithelium and oedematous areas in the dermis was observed. In the VAT group, these findings were significantly improved. Conclusion: We demonstrated that adenosine triphosphate can prevent vandetanib-induced skin toxicity in rats for the first time. The promising results denote that further studies testing this agent in other animal models and in humans are warranted.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2020Effect of rutin on cytarabine-associated pulmonary oedema and oxidative stress in rats
Bilgin, Asli O.; Mammadov, Renad; Suleyman, Bahadir; Unver, Edhem; Ozcicek, Fatih; Soyturk, Mehmet; Cimen, Ferda K.; Kurt, Nezahat; Suleyman, Halis
Cytarabine is effectively used in the treatment of adult acute leukemia, but it has a dose-limiting side effect of fatal pulmonary oedema because it increases the vascular permeability of the alveolar capillaries. The aim of the present study was to conduct a radiological, biochemical and histopathological investigation of the effect of rutin on cytarabine-associated pulmonary oedema in rats. Rats were treated with a combination of rutin+cytarabine by administering oral rutin at a dose of 50 mg/kg; other rat groups were orally administered the same volume of physiological saline. One hour after administration of rutin or saline, the rutin+cytarabine and cytarabine groups received an intraperitoneal injection of cytarabine (200 mg/kg). This administration procedure was repeated once a day for 14 days. Radiologically, 50% of the animals given cytarabine alone showed lung oedema, but the rutin+cytarabine group showed no oedema. The inclusion of rutin decreased the amounts of cytarabine-associated malondialdehyde, tumour necrosis factor-α, and nuclear factor-κB in the lung tissue. Rutin also inhibited the reduction of total glutathione by nitric oxide. These findings suggest that rutin may be a beneficial adjunct that can minimise the development of cytarabine-associated pulmonary oedema.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2019Effect of benidipine on experimental gastric ulcers in rats
Kuzucu, Mehmet; Suleyman, Bahadir; Mammadov, Renad; Ozcicek, Adalet; Ozcicek, Fatih; Altuner, Durdu; Süleyman, Zeynep
Peptic ulcer has been reported to increase acid secretion and lead to oxidative stress. Benidipine is an antihypertensive drug with antioxidant properties. This study aims to investigate the effects of benidipine on indomethacin-induced gastric ulcers in rats. Four groups were designed in this study. Gastric ulcer was occurred with indomethacin in the first three groups. These groups were treated with famotidine, benidipine and distilled water respectively 5 minutes before indomethacin administration. The fourth group rats didn’t have gastric ulcer and they received only distilled water. Six hours after drug administration gastric tissue was extracted and macroscopic and biochemical examinations were performed. Damaged areas in the stomach of benidipine and famotidine receiving animal groups were smaller than the indomethacin received animals. Indomethacin elevated the levels of malondialdehyde and myeloperoxidase in the stomach tissue (p<0.0001), and also decreased glutathione, glutathione related enzymes and superoxide dismutase (p<0.0001). Benidipine may be useful in preventing the toxic effect of indomethacin on the stomach.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2019Protective effect of taxifolin on cisplatin-induced nephrotoxicity in rats
Kara, Ali Veysel; Aldemir, Mehmet Naci; Ozcicek, Fatih; Mammadov, Renad; Yazıcı, Gulce Naz; Sunar, Mukadder; Gulaboglu, Mine
OBJECTIVE: To show the protective effects of taxifolin on cisplatin-induced oxidative renal injury. STUDY DESIGN: Rats were divided into 3 groups: the healthy group, the cisplatin group (2.5 mg/kg cisplatin only), and the taxifolin-cisplatin group (50 mg/kg taxifolin+2.5 mg/kg cisplatin). The rats were sacrificed after 14 days, and the kidneys were removed for examination of malondialdehyde (MDA), total glutathione (tGSH), and super oxide dismutase (SOD) levels. Blood urea nitrogen (BUN) and creatinine levels were measured in the blood samples taken before the animals were sacrificed. Kidney tissues were examined histopathologically. Finally, biochemical and histopathological results of the groups were compared. RESULTS: Cisplatin significantly increased MDA and decreased tGSH and SOD in the rat kidney tissue (p<0.001). Additionally, cisplatin caused an increase in serum creatinine and BUN levels (p<0.001). Taxifolin prevented the cisplatin-induced increase in MDA and decrease in tGSH and SOD (p<0.001). It also decreased serum creatinine and BUN levels significantly as compared with the cisplatin group (p<0.001). In the cisplatin group microscopic examinations showed obvious kidney damage including dilation, severe necrosis, and degenerative changes. Taxifolin prior to cisplatin markedly ameliorated these changes. CONCLUSION: We have demonstrated for the first time that taxifolin can prevent cisplatin-induced nephrotoxicity.
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