Person: ELÇİOĞLU, HATİCE KÜBRA
Loading...
Email Address
Birth Date
Research Projects
Organizational Units
Job Title
Last Name
ELÇİOĞLU
First Name
HATİCE KÜBRA
Name
23 results
Search Results
Now showing 1 - 10 of 23
Publication Metadata only Protective effects of resveratrol on hepatic ischemia reperfusion injury in streptozotocin-induced diabetic rats(SPRINGER, 2019) ELÇİOĞLU, HATİCE KÜBRA; Aktas, Hanife Serife; Ozel, Yahya; Ahmad, Sarfraz; Pence, Halime Hanim; Ayaz-Adakul, Betul; Kudas, Ilyas; Tetik, Sermin; Sekerler, Turgut; Canbey-Goret, Ceren; Kabasakal, Levent; Elcioglu, Hatice KubraResveratrol (RSV) is a natural polyphenolic compound having antioxidant effects. This study was designed to investigate the protective effects of resveratrol against oxidative stress in hepatic ischemia-reperfusion (I/R) injury in streptozotocin (STZ)-induced diabetic rats. STZ was injected intraperitonally (i.p.) to 18 Sprague-Dawley albino rats, which were divided into three groups, each having six rats. First group was non-treated diabetic group (D), second diabetic group was subjected to 30 min of hepatic ischemia followed by a 45-min reperfusion period (D + I/R), and third diabetic group was subjected to 30 min of hepatic ischemia followed by a 45-min reperfusion period and treated with 20 mg/kg/day oral RSV before 30 min I/R injury (D + I/R + RSV). At the end of the experimental period, animals were decapitated, and blood samples were collected to determine tissue tumor necrosis factor-alpha (TNF-alpha) levels. Liver and lung tissue samples were obtained for the evaluation of biochemical parameters including malondialdehyde (MDA) and glutathione (GSH) levels and histopathological examinations. Compared to control, I/R injury resulted in decreases in GSH levels and increases in MDA levels. Tissue TNF-alpha levels were also increased in the D + I/R group compared to D group. Treatment with RSV prevented the alterations on biochemical parameters and histopathological changes induced by I/R. We demonstrate that in diabetic rats, hepatic I/R injury is associated with an augmented inflammatory response and oxidative stress, while RSV pre-treatment significantly decreased these responses. Larger clinical studies are desirable to determine the exact role(s) of RSV on hepatic I/R injury among diabetic subjects.Publication Metadata only Octreotide ameliorates alendronate-induced gastric injury(ELSEVIER SCIENCE INC, 2004) ŞENER, GÖKSEL; Sener, G; Paskaloglu, K; Kapucu, C; Cetinel, S; Contuk, G; Ayanoglu-Dulger, GAlendronate causes serious gastrointestinal adverse effects. The aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue, improves the alendronate-induced gastric injury. Rats were administered 20 mg/kg alendronate by gavage for 4 days, either alone or following treatment with octreotide (0.1 ng/kg, i.p.). On, the last day, following drug administration, pilor ligation was performed and 2 h later,rats were killed and stomachs were removed. Gastric acidity and tissue ulcer index values, lipid peroxidation (as assessed by malondialdehyde, MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity as well as the histologic appearance of the stomach tissues were determined. Chronic oral administration of alendronate induced significant gastric damage, increasing lipid peroxidation (37.1 +/- 3.2 nmol/g) and myeloperoxidase activity (57.6 +/- 3.7 U/g), while tissue glutathione levels (0.9 +/- 0.1 mumol/g) decreased. Treatment with octreotide prevented this damage as well as the changes in biochemical parameters (MDA: 23.4 +/- 1.3 nmol/g; MPO: 31.68 U/g; GSH: 1.5 +/- 0.1 mumol/g). Findings of the present study suggest that alendronate induces oxidative gastric damage by a local irritant effect, and that octreotide ameliorates this damage by inhibiting neutrophil infiltration and reducing lipid peroxidation. Therefore, its therapeutic role as a ulcer healing agent must be further elucidated in alendronate-induced gastric mucosal injury. (C) 2004 Elsevier Inc. All rights reserved.Publication Metadata only Protective effect of famotidine, omeprazole, and melatonin against acetylsalicylic acid-induced gastric damage in rats(2001) ELÇİOĞLU, HATİCE KÜBRA; Sener-Muratoğlu, G.; Paskaloğlu, K.; Arbak, S.; Hürdağ, C.; Ayanoğlu-Dülger, G.It has been reported that both omeprazole and famotidine have a protective effect against gastric mucosal damage induced by acetylsalicylic acid (ASA) and other nonsteroidal anti-inflammatory drugs. Since active oxygen species and lipid peroxidation were reported to play a role in the pathogenesis induced by ASA, we aimed to study if omeprazole and famotidine have any antioxidant effect by comparing their protective effect with that of melatonin, an effective antioxidant and free radical scavenger. Mucosal damage was evaluated by macroscopic examination, histological analysis and by measurement of lipid peroxidation (LPO), glutathione (GSH), and myeloperoxidase (MPO) activity. Omeprazole (20 micromol/kg per os), famotidine (3 mg/kg per os), and melatonin (10 mg/kg intraperitoneally) significantly prevented gastric ulcerogenesis induced by ASA (200 mg/kg per os) and decreased the ulcer index. Gastric LPO and MPO activity that were increased significantly by ASA were decreased after treatment with omeprazole, famotidine, and melatonin. ASA treatment decreased significantly the gastric GSH levels, and pretreatment with omeprazole, famotidine, or melatonin increased it significantly. Famotidine and omeprazole decreased the gastric acidity, which was increased by ASA, whereas melatonin had no effect on this parameter. These findings suggest that active oxygene species and LPO have an important role in the pathogenesis of gastric mucosal damage induced by ASA and that both famotidine and omeprazole may be protective against this damage, although they were not as efficient as melatonin as an antioxidant. On the other hand, the antisecretory effect of omeprazole and famotidine may also be contributing to their antiulcer effect.Publication Metadata only Effects of systemic Thalidomide and intracerebroventricular Etanercept and Infliximab administration in a Streptozotocin induced dementia model in rats(ELSEVIER GMBH, 2015) ELÇİOĞLU, HATİCE KÜBRA; Elcioglu, H. Kubra; Kabasakal, Levent; Tufan, Fatih; Elcioglu, Omer H.; Solakoglu, Seyhun; Kotil, Tugba; Karan, Mehmet AkifTumor necrosis factor-alpha (TNF-alpha) upregulation enhances amyloid beta (AP beta) induced neurotoxicity in Alzheimer's disease (AD). Intracerebroventricular streptozotocin (STZ) administration causes pathological changes and cognitive deficits similar to those seen in AD by causing impairment of brain glucose and energy metabolism. Recent reports indicate a protective role of Thalidomide. Etanercept, and Infliximab, all of which have anti-TNF-alpha activity, against cognitive and neuropathological changes in experimental and clinical studies. We aimed to investigate the protective effects of Thalidomide, Etanercept, and Infliximab in a rat model of intracerebroventricular STZ-induced dementia. Sprague-Dawley rats (250-300 g) were separated to sham (n = 6) and STZ (n = 24) groups. The STZ group was divided into four groups (STZ, STZ-thalidomide, STZ-etanercept, and STZ-infliximab). Morris's water maze (MWM) and passive avoidance (PA) tests were performed. At the end of the third week, brain tissues were obtained. Histopathological analysis, immunohistochemistry, and electron microscopic examinations were done. The improvement performance of the STZ group was significantly reduced in the MWM test (p < 0.001). Compared with the STZ, STZ-thalidomide, STZ-etanercept, and STZ-infliximab groups had significantly better performance (p < 0.001. <0.05 and <0.05, respectively) in the MWM test. STZ administration caused a significant decrease in the mean escape latency in PA reflex (p < 0.001). Thalidomide, Etanercept, and Infliximab were associated with better PA reflexes compared to the STZ group (p < 0.001 for all). Morphological and immunohistochemical results showed increased neurodegenerative changes compared to sham group. Our findings are in line with the findings reported in the literature and encourage further studies with TNF-alpha antagonists, in particular Thalidomide. (C) 2015 Elsevier GmbH. All rights reserved.Publication Open Access The effects of Origanum onites in streptozotocin-induced diabetes mellitus in rats(2022-01-01) POLAT, ELİF BEYZANUR; TAŞKIN, TURGUT; BİTİŞ, LEYLA; ELÇİOĞLU, HATİCE KÜBRA; Aydemir O., Polat E. B. , Aljesri K., TAŞKIN T., BİTİŞ L., ELÇİOĞLU H. K.© 2022 Marmara University Press.Diabetes mellitus is a chronic disease characterized by decreased insulin synthesis and/or increased blood glucose due to insulin resistance. In this study, streptozotocin (STZ)-induced diabetic rats were evaluated and it was aimed to investigate the protective effects of Origanum onites L. (OO) against possible changes in these parameters. Male Sprague-Dawley rats weighing 300-400g were divided into three groups control (C), diabetes mellitus (DM) and diabetes mellitus + OO (OO group). DM was induced by administration of STZ 60 mg/kg dose intraperitoneally (i.p.) after 48 hours, rats with blood glucose values higher than 200 mg/dL were considered DM. Origanum extract was administered i.p. to the OO group at 50 mg/kg per day for 6 weeks. Serum AST, ALT, creatinine, and inflammatory cytokine levels were measured. MDA and GSH levels were measured in liver tissues. AST, ALT, creatinine, and MDA levels were found to be increased in the DM group, while a significant decrease in these levels was observed in the treated group. While GSH values fell in the DM group, a significant increase occurred in the OO group (n=6, p<0.0001; two-way ANOVA). When the plasma levels of cytokines were examined, an increase was observed in the DM group and a significant decrease was observed in the OO group. When we evaluate our findings, we think that OO has a protective effect against complications that may occur in DM by preventing oxidant damage and inflammation. Further studies are needed on the protective effects of OO in DM.Publication Metadata only Melatonin protects against gentamicin-induced nephrotoxicity in rats(2002) ŞENER, GÖKSEL; Sener, Göksel; Sehirli, A. Ozer; Altunbas, Hale Z.; Ersoy, Yasemin; Paskaloglu, Kübra; Arbak, Serap; Ayanoglu-Dulger, GülAcute renal failure is a major complication of gentamicin (GEN), which is widely used in the treatment of gram-negative infections. A large body of in vitro and in vivo evidence indicates that reactive oxygen metabolites (or free radicals) are important mediators of gentamicin nephrotoxicity. In this study we investigated the role of free radicals in gentamicin-induced nephrotoxicity and whether melatonin, a potent antioxidant could prevent it. For this purpose female Sprague-Dawley rats were given intraperitoneally either gentamicin sulphate (40 mg/kg), melatonin (10 mg/kg), gentamicin plus melatonin or vehicle (control) twice daily for 14 days. The rats were decapitated on the 15th day and kidneys were removed. Blood urea nitrogen (BUN) and creatinine levels were measured in the blood and malondialdehyde (MDA) and glutathione (GSH) levels, protein oxidation (PO) and myeloperoxidase (MPO) activity were determined in the renal tissue. Gentamicin was observed to cause a severe nephrotoxicity which was evidenced by an elevation of BUN and creatinine levels. The significant decrease in GSH and increases in MDA levels, PO and MPO activity indicated that GEN-induced tissue injury was mediated through oxidative reactions. On the other hand simultaneous melatonin administration protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by GEN treatment.Publication Metadata only Thalidomide attenuates learning and memory deficits induced by intracerebroventricular administration of streptozotocin in rats(TAYLOR & FRANCIS LTD, 2013) ELÇİOĞLU, HATİCE KÜBRA; Elcioglu, H. K.; Kabasakal, L.; Alan, S.; Salva, E.; Tufan, F.; Karan, M. A.Neuroinflammatory responses caused by amyloid beta (A beta) peptide deposits are involved in the pathogenesis of Alzheimer's disease (AD). Thalidomide has a significant anti-inflammatory effect by inhibiting TNF-alpha, which plays role in A beta neurotoxicity. We investigated the effect of thalidomide on AD-like cognitive deficits caused by intracerebroventricular injection of streptozotocin (STZ). Intraperitoneal thalidomide was administered 1 h before the first dose of STZ and continued for 21 days. Learning and memory behavior was evaluated on days 17, 18 and 19, and the rats were sacrificed on day 21 to examine histopathological changes. STZ injection caused a significant decrease in the mean escape latency in passive avoidance and decreased improvement of performance in Morris water maze tests. Histopathological changes were examined using hematoxylineosin and Bielschowsky staining. Brain sections of STZ treated rats showed increased neurodegeneration and disturbed linear arrangement of cells in the cortical area compared to controls. Thalidomide treatment attenuated significantly STZ induced cognitive impairment and histopathological changes. Thalidomide appears to provide neuroprotection from the memory deficits and neuronal damage induced by STZ.Publication Metadata only Changes in caveolin-1 expression and vasoreactivity in the aorta and corpus cavernosum of fructose and streptozotocin-induced diabetic rats(ELSEVIER, 2010) ELÇİOĞLU, HATİCE KÜBRA; Elcioglu, Kuebra H.; Kabasakal, Levent; Cetinel, Sule; Conturk, Gazi; Sezen, Sena F.; Ayanoglu-Dulger, GuelHyperglycemia is a common defining feature in the development of endothelial dysfunction which plays a key role in the pathogenesis of both type 1 and type 2 diabetes. Caveolin-1 is the main structural component of caveolae which might be involved in the pathophysiology of macrovascular complications of diabetes. In this study we aimed to observe the effect of caveolin-1 on functional responses of aorta and corpus cavernosum in the streptozotocin and fructose-induced diabetes groups. Type 1 diabetes was induced by intraperitoneal administration of streptozotocin (60 mg/kg),. Type 2 diabetes by adding fructose in the rat's drinking water (10% (w/v)) for 8 weeks. For insulin treatment; rats were treated with insulin (6 U/kg) for 8 weeks. In Type I and Type II diabetic groups the contractile responses of corpus cavernosum strips to phenylephrine (EC50:1.82 x 10(-5) M;1.47 x 10(-5) M, respectively)and relaxation responses to acetylcholine (EC50:7.5 x 10(-5) M;4.48 x 10(-5) M, respectively)were significantly impaired. Contractile responses of aortic-strips to phenylephrine in diabetic groups were markedly decreased (EC50:3.7. 10(-7) M;2.61. 10(-7) M respectively) and dose-dependent relaxation responses to acetylcholine were also attenuated (EC50:3.23 . 10(-6)M; 2.0. 10(-6)M respectively). Treatment with insulin improved the functional responses in the aorta and corpus cavernosum. Protein expression of caveolin-1 was increased in the aorta and corpus cavernosum of the diabetic groups, but this increase seen in the streptozotocin group was more significant than the fructose group. Our findings indicate that an attenuation of the functional responses in both diabetes groups were probably associated with an enhanced expression of caveolin-1, and therefore a decrease in the eNOS activity with a concomitant decrease in NO synthesis. (C) 2010 Elsevier B.V. All rights reserved.Publication Open Access Evaluation of the design and methodology of applications to the local ethics committee(2021-10-01) ELÇİOĞLU, HATİCE KÜBRA; ALTUNTAŞ Y., YILDIRMAK Z. Y. , ERDOĞAN M. S. , SEÇKİN D., AKSU ÇERMAN A., YAPIŞLAR H., ÖNAL F. G. , ELÇİOĞLU H. K. , EREN N., Necioglu Orken D.Objectives: Proposals for scientific studies must have an original hypothesis and the appropriate design and methodology to test the premise. Methods: This study is an evaluation of the suitability of applications submitted to a local ethics committee (EC) and the rate of publication of that research. Results: A total of 899 files submitted for EC approval were retrospectively assessed. The EC found that the description of the methods in 44% of the applications was inaccurate, and that this type of error was most often seen in submissions from the surgical branch. In all, 52% of the applications for which we were informed about their final status were not published. Conclusion: The results suggest that improved training in epidemiology is required to reduce the number of application errors and that new regulations could help to motivate healthcare personnel to conduct scientific research and publish their findings. Keywords: Case-control study; epidemiology; ethics committees; interventional studies; research misconduct; thesis studiesPublication Metadata only Ischemic colitis of the colon in streptozotocin-induced diabetic rats(SPRINGER, 2018) ELÇİOĞLU, HATİCE KÜBRA; Ozel, Yahya; Elcioglu, H. Kubra; Cevikelli, Z. Ayca; Kudas, Ilyas; Ahmad, Sarfraz; Uzun, Hafize; Topal, Cumhur; Aktas, Serife; Kabasakal, LeventThis study focuses on two inflammatory diseases, viz., diabetes mellitus (DM) that causes serious complications such as retinopathy, nephropathy, and neuropathy, and ischemic colitis which is evoked by DM. Ischemic colitis originates from the reduction in mesenteric blood flow to the colon with existence of the occlusive or non-occlusive reasons. Our study objective was to provide early diagnostic approach for ischemic colitis in streptozotocin (STZ)-induced diabetic rats. Sprague-Dawley rats were divided into four groups: (i) control use of 0.1 M citrate buffer, the solvent of streptozotocin (C), (ii). induced ischemia (I), (iii) rats subjected to 60 mg/kg STZ intraperitoneally to induce type 1 diabetes (D) (48 h after STZ injection, blood glucose levels >200 mg/dl were considered as diabetic), and (iv) diabetic rats subjected to intestinal ischemia (D+I). The third diabetic group (D) was not operated. At the end of the experimental period, rats were sacrificed, C-reactive protein (CRP) and calprotectin levels were measured in the serum and colon tissue specimens. Tissue specimens were also analyzed histologically. We found that serum and colon calprotectin levels were elevated in the D+I group compared to the D and/or I group alone, but relatively calprotectin levels increased in I as compared to C group in colon tissues. CRP levels were significantly increased with ischemic colitis in diabetes, while colon CRP levels were decreased. These results provide evidence for the existence of inflammation in the STZ-induced diabetic rats with ischemic colitis. In conclusion, our measurements of serum calprotectin levels of STZ-induced diabetic rats with ischemic colitis provide a practical approach for an early diagnosis of ischemic colitis. Furthermore, these biochemical analyses correlate well with the histopathologic findings of STZ-induced diabetic rats with ischemic colitis. Future studies would be desirable to further strengthen the role of calprotectin in the early diagnosis of ischemic colitis in diabetics clinical settings.
- «
- 1 (current)
- 2
- 3
- »