Sürdürülebilir Kalkınma Amaçları

  • ArticleAçık Erişim2022
    Effect of taxifolin on methotrexate-induced oxidative and inflammatory oral mucositis in rats: biochemical and histopathological evaluation

    Bayramoglu, Zeynep; Mokhtare, Behzad; Mendil, Ali Sefa; Coban, Taha Abdulkadir; Mammadov, Renad; Bulut, Seval; Suleyman, Zeynep; Suleyman, Halis

    The role of oxidative stress, as well as inflammation in the pathogenesis of methotrexate (MTX)-induced oral mucositis, is a known fact. The anti-inflammatory, antitumor, antimicrobial, and antioxidant properties of taxifolin—the effect we tested against MTX-induced oral mucosal damage—are well known. Objective: Evaluating biochemically and histopathologically the effects of taxifolin on methotrexate-induced oral mucosal damage in rats. Methodology: In the taxifolin+MTX (TMTX) group, 50 mg/kg taxifolin was orally administered to rats by gavage. In the MTX and healthy (HG) groups, normal saline was applied to rats as solvent by the same method. One hour after administration of taxifolin and solvent, 5 mg/kg MTX was orally administered to rats in the MTX and TMTX groups. Taxifolin and methotrexate were administered once a day for 30 days. Macroscopic, biochemical, and histopathological evaluations were performed on the inner cheek and tongue tissues of rats. These parts were removed after rats were killed with a high-dose anesthesia. Results: Taxifolin with MTX prevented the increase in oxidant and pro-inflammatory parameters, such as malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), on the inner cheek and tongue tissues of rats. Moreover, taxifolin antagonized the decrease in total glutathione (tGSH). Taxifolin decreased MTX-induced histopathological damage. Conclusion: These findings suggest that taxifolin may be useful to treat MTX-associated oral mucositis.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2022
    Molecular Mechanism and Pathogenesis-Oriented Treatment of Antipsychotic Drug-Induced Infertility in Female Rats

    Ozyurt, Ramazan; Suleyman, Halis; Dinc, Kemal; Yildiz, Sevler; Coban, Taha Abdulkadir; Bulut, Seval; Suleyman, Zeynep; Altuner, Durdu; Keskin, Deha Denizhan; Keskin, Seda

    Typical and atypical antipsychotics may cause subfertility through oxidative stress in reproductive cells and endocrine axis. This experimental study was designed to determine the effects of adenosine triphosphate (ATP) treatment on oxidative stress markers and hyperprolactinemia in subfertility due to antipsychotics. A total of 54 Albino Wistar female rats were divided into nine groups as the healthy (HG), haloperidol (HPL), olanzapine (OLZ), clozapine (CLZ), aripiprazole (ARZ), ATP+haloperidol (ATP+HPL), ATP+olanzapine(ATP+OLZ), ATP+clozapine (ATP+CLZ) and ATP+aripiprazole (ATP+ARZ) groups. ATP was injected intraperitoneally (ip) at a dose of 25 mg/kg to animals in ATP+HPL, ATP+OLZ, ATP+CLZ, and ATP+ARZ groups. HG, HPL, OLZ, CLZ, and ARZ groups were given the same volume of distilled water via ip. One hour after administration of drugs and solvent, haloperidol (2 mg/kg) for ATP+HPL and HPL groups, olanzapine (2 mg/kg) for ATP+OLZ and OLZ groups, clozapine (20 mg/kg) for ATP+CLZ and CLZ groups and aripiprazole (3 mg/kg) for ATP+ARZ and ARZ groups was given orally to by gavage. This procedure was repeated once a day for 15 days. After this period, blood samples were taken for oxidant, antioxidant and prolactin measurement and the animals were kept with mature male rats for one month for breeding. The degree of oxidative stress, hyperprolactinemia and subfertility caused by antipsychotics were found to be haloperidol, olanzapine, clozapine, aripiprazole, in order of frequency. ATP administration reversed the increase in oxidants markers and the decrease of antioxidants significantly. ATP administration prevents subfertility due to antipsychotic drugs.

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  • ArticleYalnız künye2022
    The Effect of Adenosine Triphosphate, Benidipine, Sugammadex, and their Combinations upon Cardiac Damage after Temporary Clamping of the Abdominal Aorta in Rats

    Emir, Izzet; Altuner, Durdu; Gulaboglu, Mine; Coban, Taha Abdulkadir; Suleyman, Bahadir; Mammadov, Renad; Ozkaraca, Mustafa; Suleyman, Zeynep; Karakurt, Tulay Ceren Olmezturk; Suleyman, Halis

    The aim of our study was to biochemically and histopathologically investigate the protective effect of adenosine triphosphate (ATP), benidipine, sugammadex and (ATP + benidipine + sugammadex) ABS against cardiac damage induced by abdominal clamping and unclamping (ACU) procedure in rats. Rats utilized were divided into six groups as Healthy (HG), Abdominal ACU (AACC), ATP + AACU (ATPG), Benidipine + AACU (BNDG), Sugammadex + AACU (SDXG), ABS + AACU (ABSG). One hour before anesthesia, ATP (25 mg/kg; ip) was administered to the ATPG group, Benidipine (4 mg/kg orally) was administered to the BNDG group, Sugammadex (4 mg/kg ip) was administered to the SDXG and ABS was administered with this specified dose and method to the ABSG group. Distilled water as a solvent was injected to AACC and HG groups. One hour after, laparotomy was performed to the rats, and the abdominal cavity was reached. Ischemia was provided for one hour and then reperfusion for 2 h placing an atraumatic clamp on the suprarenal abdominal aorta of the animals in all groups (except from the HG). The heart tissues extracted from the killed animals were examined biochemically and histopathologically. ATP and benidipine suppressed the increase of oxidant and proinflammatory cytokines better than sugammadex. The ABSG group was found to be almost the same as the healthy group biochemically and histopathologically (p > 0.05). ABS drug form alone was possible to be much more beneficial rather than ATP, benidipine and sugammedex in the treatment of cardiac damage induced by AACU procedure.

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  • ArticleAçık Erişim2022
    Amelioration 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.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2022
    Effect 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.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2021
    The effect of adenosine triphosphate on propofol-induced myopathy in rats: A biochemical and histopathological evaluation

    Erdem, Kezban Tuna Ozkaloglu; Bedir, Zehra; Ates, Irem; Kuyrukluyildiz, Ufuk; Coban, Taha Abdulkadir; Yazici, Gulce Naz; Arslan, Yusuf Kemal; Suleyman, Zeynep; Suleyman, Halis

    Propofol infusion syndrome characterized by rhabdomyolysis, metabolic acidosis, kidney, and heart failure has been reported in long-term propofol use for sedation. It has been reported that intracellular adenosine triphosphate (ATP) is reduced in rhabdomyolysis. The study aims to investigate the protective effect of ATP against possible skeletal muscle damage of propofol in albino Wistar male rats biochemically and histopathologically. PA-50 (n = 6) and PA-100 (n = 6) groups of animals was injected intraperitoneally to 4 mg/kg ATP. An equal volume (0.5 ml) of distilled water was administered intraperitoneally to the P-50, P-100, and HG groups. One hour after the administration of ATP and distilled water, 50 mg/kg propofol was injected intraperitoneally to the P-50 and PA-50 groups. This procedure was repeated once a day for 30 days. The dose of 100 mg/kg propofol was injected intraperitoneally to the P-100 and PA-100 groups. This procedure was performed three times with an interval of 1 days. Our experimental results showed that propofol increased serum CK, CK-MB, creatinine, BUN, TP I, ALT, AST levels, and muscle tissue MDA levels at 100 mg/kg compared to 50 mg/kg and decreased tGSH levels. At a dose of 100 mg/ kg, propofol caused more severe histopathological damage compared to 50 mg/ kg. It was found that ATP prevented propofol-induced muscle damage and organ dysfunction at a dose of 50 mg/kg at a higher level compared to 100 mg/kg. ATP may be useful in the treatment of propofol-induced rhabdomyolysis and multiple organ damage.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2021
    Valeriana officinalis is Effective on Stress-Induced Infertility, Delayed Maternity, and Intrauterine Growth Restriction of the Fetus in Female Rats

    Uzel, Kemine; Turkler, Can; Mammadov, Renad; Yazici, Gulce Naz; Arslan, Yusuf Kemal; Coban, Taha Abdulkadir; Suleyman, Zeynep; Gursul, Cebrail; Suleyman, Halis

    SUMMARY. Infertility is a tragic option for reproductive-aged women. About 20 % of lost ability to conceive are caused by unexplained etiology. Some of these cases are linked with psychological stress. It can cause depression and anxiety, and the latter can cause infertility. The therapy with sedative, antidepressant, anxi-olytic and antioxidant effects may be beneficial in preventing infertility caused by psychological disorders and maintaining normal intrauterine physical development of the fetus. The aim of our study is to investi-gate the protective effect of Valeriana plant root extract against stress-induced reproductive disorders. The protective effect of Valeriana plant root extract against infertility and delayed maternity was investigated in a stress model induced by the forced immobilization method in albino Wistar female rats and compared with ascorbic acid. Valeriana officinalis plant root extract was effective against psychological stress-related infertility and delayed maternity, ascorbic acid was found to be ineffective. This information suggests that psychological stress-related ovarian damage, infertility, delayed maternity, and great obstetric syndromes are based on the role of psychological disorders such as anxiety and depression rather than oxidative stress. Our experimental results indicate that Valeriana officinalis plant root extract can be useful in the treatment of stress-related ovarian damage and reproductive disorders.

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  • ArticleAçık Erişim2021
    Protective effect of lutein against acrolein-induced ototoxicity in rats

    Erhan, Ertugrul; Salcan, Ismail; Bayram, Rana; Suleyman, Bahadir; Dilber, Muhammet; Yazici, Gulce Naz; Coban, Taha Abdulkadir; Altuner, Durdu; Suleyman, Halis

    Background: Acrolein is a reactive aldehyde that forms during burning of wood and other fuels. It is also a product of lipid peroxidation (LPO) reactions and is present in cigarette smoke. Acrolein is known to cause oxidative stress and inflammatory nerve tissue damage. Lutein is a tetraterpenoid molecule with antioxidant and anti-inflammatory properties. There appear to be no studies on the effect of lutein on vestibulocochlear nerve damage induced by acrolein. The aim of this study was to investigate the effect of lutein on vestibulocochlear nerve damage induced by acrolein in rats using biochemical and histopathological methods. Methods: The rats were divided into three groups (n = 6, for each group) a healthy control group (HG), an acrolein (ACR) group and a lutein and acrolein (LACR) group. In the LACR group, lutein was administered (1 mg/kg) via oral gavage. The ACR and HG groups received saline via oral gavage. Then, 1 h after the administration of lutein and saline, the LACR and ACR groups were treated with 3 mg/kg of acrolein via oral gavage. This procedure was repeated once a day for 30 days. Results: The results of biochemical experiments showed that in the vestibulocochlear nerve tissues of the animals treated with acrolein, the levels of malondialdehyde, total oxidants, nuclear factor kappa b, tumor necrosis factor alpha and interleukin 1 beta significantly increased, whereas the levels of total glutathione and total antioxidants decreased as compared to those in the HG and LACR groups. In addition, severe histopathological damage was observed in vestibulocochlear nerve tissue of the acrolein group, whereas this damage was alleviated in the lutein group. Conclusion: Lutein protected vestibulocochlear nerve tissue from acrolein-associated oxidative and proinflammatory damage. This suggests that lutein might be useful in preventing or treating acrolein-induced ototoxicity.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2021
    How do routine laboratory tests change in coronavirus disease 2019?

    Mertoglu, Cuma; Huyut, Mehmet Tahir; Arslan, Yusuf; Ceylan, Yasar; Coban, Taha Abdulkadir

    How the routine laboratory tests change in terms of coronavirus disease 2019 (COVID-19) was retrospectively analyzed in a large group of patients. Biochemical, hematological and inflammatory variables of a totaly 555 (n = 532 in non-intensive care unit (non-ICU), n = 23 in ICU) patients diagnosed with COVID-19 were analyzed accessing them through the laboratory information system. White blood cell (WBC), neutrophil (NEU), platelet large cell ratio, neutrophil to lymphocyte ratio (NLR), derived NLR (d-NLR), aspartate aminotransferase, urea, creatine kinase (CK) myocardial band (CK-MB), procalcitonin (PCT) values were high whereas lymphocyte (LYM), eosinophil, red blood cells (RBC), hemoglobin, lymphocyte to monocyte ratio, estimated glomerular filtration rate values were low in the ICU group when compared with non-ICU. WBC, NEU, red cell distribution width, alanine transaminase, creatinine, urea, CK-MB, CK, direct bilirubin, lactate dehydrogenase, glucose, C-reactive protein, erythrocyte sedimentation rate, ferritin, D-dimer, PCT and international normalized ratio values increased while RBC, hemoglobin, hematocrit, mean corpuscular volume and total bilirubin values decreased in a significant proportion of patients in both groups based on the normal reference ranges. LYM count was found to be low in a significant number of patients (57.5%) especially in the ICU group and as an important risk factor and diagnostic parameter on admission to ICU (OR: 125, AUC: 0.74). Routine laboratory tests provide important information in terms of both diagnosis and severity of COVID-19. Lymphopenia is a condition that should be monitored which indicates the severity of the disease.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2021
    The Effect of Taxifolin on Acrylamide-induced Oxidative and Proinflammatory Brain Injury in Rats: A Biochemical and Histopathological Study

    Ersoy, Alevtina; Yasar, Hasan; Tanoglu, Ceyda; Yazici, Gulce Naz; Coban, Taha Abdulkadir; Arslan, Yusuf Kemal; Suleyman, Halis

    Purpose: Acrylamide is a well-known environmental toxic compound. Taxifolin belongs to the group of flavonoids that have antioxidant, antimicrobial, anti-inflammatory and anti-carcinogenic properties. In this study, we investigated the effect of taxifolin on acrylamide-related oxidative and proinflammatory brain damage. Methods: The experimental animals were divided into three groups: (1) those treated with acrylamide 20 mg/kg p.o., (2) those treated with taxifolin 50 mg/kg p.o. and acrylamide and (3) the control group. At the end of the experiment, the rat brain tissues were examined for the levels of Malondialdehyde (MDA), total glutathione (tGSH), tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). A histopathological analysis was performed to detect the morphological changes in the brain. Results: Exposure to acrylamide caused a significant increase in the levels of MDA, TNF-α and IL-1β and a decrease in the values of tGSH, which indicates the presence of oxidative stress and inflammation in the brain tissue. Taxifolin treatment significantly reduced the levels of MDA and TNF-α and brought the mean values of IL-1β and tGSH close to those of the control group. The group that received acrylamide exhibited histopathological changes, such as neuronal degeneration, edema of microglia, dilated and congestive vessels and apoptotic inclusion. The use of taxifolin significantly improved the morphological changes in the brain tissue of the acrylamide-exposed rats. Conclusion: Acrylamide causes brain damage, inducing oxidative stress and inflammation. Due to its antioxidant and anti-inflammatory properties, taxifolin may be one of the agents that can reduce the neurotoxic effects of acrylamide.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2021
    The effect of adenosine triphosphate on oral mucosity in rats due to sunitinib administration

    Dilber, Muhammet; Salcan, Ismail; Bayram, Rana; Suleyman, Esma; Yildirim, Ugur; Sonmez, Faik; Bakan, Ebubekir; Coban, Taha Abdulkadir; Suleyman, Zeynep; Suleyman, Halis

    Sunitinib, a common drug used in cancer treatment, is a multi-targeted tyrosine kinase in-hibitor. It is argued that sunitinib-associated oral mucositis is caused by VEGF inhibition. Previous research has documented that ATP allows for wound healing through an increase in VEGF levels and pro-vides an antioxidant effect. The aim of our study was to biochemically analyze whether adenosine triphos-phate (ATP) offers any protective effects against potential oral oxidative mucosal damage due to sunitinib use in male albino Wistar rats. ATP was injected ip at 25 mg/kg dose to sunitinib + ATP(SAT) (n=8) group. Normal saline (0.9% NaCl) was applied in the same route to the sunitinib-alone(SUN) (n=8) and healthy (HG) (n=8) groups as the solvent. One hour after ATP and 0.9% NaCl were administered, oral de-livery of 25 mg/kg sunitinib was given to the SAT and SUN groups, once a day for four weeks. While MDA, TOS and 8-OHdG levels were significantly higher (p < 0.001) compared to the healthy and ATP group in the oral cavity tissues of subjects treated with sunitinib, tGSH and TAS were significantly lower (p < 0.001). Our experimental results show that ATP protects tongue and cheek tissues of rats from oxida-tive damage of sunitinib, indicating that ATP may be beneficial for sunitinib-related oral mucosal injury.

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  • ArticleAçık Erişim2020
    The Effect of Ozone Treatment on Thermal Burn Wound Healing; an Experimental Study

    Peker, Kemal; Yilmaz, Ismayil; Demiryilmaz, Ismail; Isik, Arda; Sayar, Ilyas; Gursul, Cebrail; Cankaya, Murat; Coban, Taha Abdulkadir

    Objective: Ozone has been advised as a metabolic excitative in cell, immunomodulatory agent and antioxidant enzyme actuator. The present study was performed to designate the profit of ozone therapy on the burn wound healing in the rats. Methods: 40 adult Wistar type rats divided into 4 groups: a control group (burn not created and topical and systemic agents not used), a burn group (burn created but only saline given), a burn+silver sulfadiazine group (silver sulfadiazine was applied for 21 days), a burn+ozone/oxygen mixture group (ozone/oxygen mixture was applied for 21 days).After anesthetizing, second-degree burn (2 cm2 areas) was done on the dorsal of the animals byaluminum plate in boiling hot water (100 degrees C for 15 seconds) and other groups except control group were treated topically, based on the time scheduled. Tissue samples were harvested on day 7st and 21st after burn injury. Biochemical and histological analyzes were performed in tissue and blood samples. The results were assessed with appropriate statistical tests and given as Means +/- SD. Results: The histopathologic damage level was significantly different in all groups. Fibrosis and inflamation levels decreased in ozone treatment and silver sulphadiazine groups compared to burn+normal saline group on the 21 days according to 7 days. In the ozone treatment group, Glucose 6-phosphate dehydrogenase activities were significantly higher than the silver sulfadiazine treated group. But glutathione reductase enzyme activities were lover in the ozone treated group and hydroxyproline concentration decreased in ozone group compared to burn+normal saline group on 7 and 21 days. Conclusions: Ozone has a detractive effect in the development of inflamation, fibrosis, and granulation via decreasing tissue damage and increasing the antioxidant enzyme activity on burn wound healing.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2019
    Effects of pycnogenol on ischemia/reperfusion-induced inflammatory and oxidative brain injury in rats

    Ozoner, Baris; Yuceli, Sahin; Aydin, Seckin; Yazici, Gulce Naz; Sunar, Mukadder; Arslan, Yusuf Kemal; Coban, Taha Abdulkadir; Suleyman, Halis

    Background: Ischemia/reperfusion (I/R) injury results from the onset of re-circulation following a perfusion deterioration period in the tissues, resulting in more damage than that caused by perfusion deterioration. This study aimed to determine the effects of pycnogenol on I/R injury in rat brain tissues. Methods: Eighteen albino Wistar rats were divided into three groups: I/R injury (IR, n = 6) group; I/R injury + pycnogenol (IR + P, n = 6) group; and sham group (SG, n = 6). After 30 min of transient ischemia, 24 h of reperfusion was achieved in the IR and IR + P groups. Surgical dissection, except for transient ischemia, was performed in SG. Next, histopathological and biochemical investigations were performed on brain tissues. Malondialdehyde (MDA), reduced glutathione (GSH), and glutathione peroxidase (GPO) were analyzed as oxidative stress markers; IL-1β and TNF-α were analyzed as inflammatory stress markers in biochemical tests. Results: Histopathological examination revealed normal morphology in SG and diffuse cortex damage with edema, vasopathology, and inflammatory cell infiltration in the IR group. The IR + P group showed less cortex damage, edema, and vasopathology than the IR group. The MDA, IL-1β, and TNF-α levels were significantly higher in the IR group than those in the SG group. The values of same markers for the IR + P group were significantly lower than the IR group. The GSH and GPO levels were significantly decreased with IR damage, but PYC treatment showed significant improvement in the levels. Conclusion: This study showed that the administration of pycnogenol ameliorated brain damage after I/R injury by reducing oxidative and inflammatory damage in the rat brain.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2018
    Effects of hippophae rhamnoides extract on oxidative mucosal injury induced by cisplatin in rat jejunum

    Arslan, Aynur; Ozcicek, Fatih; Cimen, Ferda Keskin; Nalkiran, Hatice Sevim; Gulaboglu, Mine; Cetin, Nihal; Coban, Taha Abdulkadir; Kuzucu, Mehmet

    Objectives: We aimed to assess the effect of Hippophae rhamnoides extract (HR) on oxidative stress induced by cisplatin (Cis) in rat small intestine tissue by evaluating the biochemical and gene expression levels and histopathological changes. Materials and methods: The control group and Cis group received distilled water, while the HR25+cisplatin (HR25+Cis) group and the HR50+cisplatin (HR50+Cis) group were given HR 25 and 50 mg/kg, respectively, orally for seven days. HR25+Cis, HR50+Cis, Cis groups were injected with a single dose of intraperitoneal cisplatin on the first day. After sacrifice, the jejunum of each rat was removed for the assessment of oxidants and antioxidants. Analyses of the gene expression (for IL-1ß and TNF-α) and histopathological changes evaluated. Results: HR significantly inhibited the increase of oxidants and the decrease of antioxidants caused by cisplatin in the jejunal tissue. IL-1β and TNF-α gene expression levels were almost the same in both the HR50+Cis and the control groups. HR better prevented increase of the serum levels of IL-1β and TNF-α in animals at 50 mg/kg dose compared to 25 mg/kg dose. We confirmed that HR prevented the histopathological changes caused by cisplatin. Conclusions: It was concluded that oxidative stress caused by cisplatin may be preventable by co-administered HR.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2018
    Does myo-inositol oxygenase, the only enzyme to catalyze myo-inositol in vivo, play a role in the etiology of polycystic ovarian syndrome?

    Mertoglu, Cuma; Gunay, Murat; Gul, Vahdet; Kulhan, Mehmet; Aktas, Mehmet; Coban, Taha Abdulkadir

    In polycystic ovary syndrome (PCOS), myo-inositol (MI) supplements have shown many beneficial effects. In this study, therefore, we aimed to investigate the serum level of myo-inositol oxygenase (MIOX), which is the only enzyme catalyzing MI in vivo, in patients with PCOS. Serum MIOX enzyme levels and other laboratory parameters were compared between sixty patients, who were diagnosed with PCOS for the first time, and sixty healthy individuals at similar age and sex. MIOX serum levels were not different between two groups (p = 0.7428). MIOX median and 95% CI were 19.4 and 10.6–39.1 in the control group and 16.4 and 7.6–46.2 in the patient group respectively. Demographic data, biochemical and hematological parameters, hormone parameters were not different except from the lymphocyte count between the two groups. Lymphocyte count was higher in the patient group. Although the ratio of LH/FSH was higher in the patient group, it was not statistically significant. Our results suggest that serum MIOX levels do not change in PCOS. It was, therefore, concluded that MI deficiency observed in PCOS was not related to the level of MIOX enzyme which cleaves MI.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2016
    Effects of nimesulide on the small intestine mucositis induced by methotrexate in rats

    Arslan, Aynur; Ozcicek, Adalet; Suleyman, Bahadir; Coban, Taha Abdulkadir; Cimen, Ferda Keskin; Nalkiran, Hatice Sevim; Kuzucu, Mehmet; Altuner, Durdu; Cetin, Nihal; Suleyman, Halis

    Intestinal mucositis is one of the major problems in the patients receiving cancer treatment. Nimesulide is a drug with antioxidant, antiinflammatory and antiulcer features. We aimed to investigate the effect of nimesulide on the small intestine mucositis induced by methotrexate (MTX) in rats. Experimental animals were divided into the control group, MTX group (MTXG) and nimesulide+MTX administered group (NMTXG) with eight rats per group. The control and MTXG groups were given distilled water by gavage and the NMTXG was given nimesulide 100 mg/kg orally. After one hour, the NMTXG and MTXG rat groups were administered oral MTX 5 mg/kg. This procedure was repeated once a day for 15 days and the rats were sacrificed. The duodenum and jejunum of each rat was removed for the assessment of biochemical markers and histopathological evaluation. Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were significantly higher in the duodenal and jejunal tissues of the animals which received MTX, compared to the control and NMTXG (P<0.001). Also, the levels of total glutathione (tGSH), glutathione reductase (GSHRd), glutathione peroxidase (GSHPx), catalase (CAT) and superoxide dismutase (SOD) were significantly lower in the MTXG (P<0.001) compared to other groups. MTX led to villus and crypt epithelial damage and inflammation containing marked PMNL and eosinophils in the intestinal tissues histopathologically. Whereas, there was only mild irregularities in the villus structures of the NMTXG. Nimesulide protected the small intestines against damage by MTX. Intestinal mucositis caused by MTX may be preventable by co-administered nimesulide.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2016
    Can thıamıne pyrophosphate prevent desflurane ınduced hepatotoxıcıty ın rats?

    Arslan, Aynur; Kuyrukluyildiz, Ufuk; Binici, Orhan; Cetin, Nihal; Balci, Mecdi Gurhan; Kuzucu, Mehmet; Yilmaz, Adnan; Altuner, Durdu; Coban, Taha Abdulkadir

    PURPOSE: To investigate the effects of thiamine pyrophosphate (TPP) against desflurane induced hepatotoxicity. METHODS: Thirty experimental animals were divided into groups as healthy (HG), desflurane control (DCG), TPP and desflurane group (TDG). 20 mg/kg TPP was injected to intraperitoneally TDG. After one hour of TPP administration, desflurane was applied for two hours. After 24 hours, liver tissues of the animals killed with decapitation were removed. The oxidant/antioxidant levels and ALT, AST and LDH activities were measured. The histopathological examinations were performed in the liver tissues for all rats. RESULTS: Notwithstanding the levels of oxidants and liver enzymes were significantly increased (p<0.0001), antioxidant levels were significantly decreased in DCG (p<0.0001). On contrary to the antioxidant parameters were increased (p<0.05) the oxidant parameters and liver enzymes were decreased in TDG (p<0.0001). Whereas multiple prominent, congestion, hemorrhage and dilatation were observed in sinusoids and lymphocyte-rich inflammation results in the centrilobular and portal areas of liver tissue in DCG, these findings were observed less frequently in TDG. CONCLUSİON: Thiamine pyrophosphate prevented liver oxidative damage induced with desflurane and may be useful in prophylaxis of desflurane induced hepatotoxicity.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2013
    Susceptibility of cord blood antioxidant enzymes glutathione reductase, glutathione peroxidase and glutathione S-transferase to different antibiotics: In vitro approach

    Ekinci, Deniz; Cankaya, Murat; Gül, Ilhami; Coban, Taha Abdulkadir

    Cord blood has numerous facilities for life and used in many different areas. Cord blood contains many different catalytic proteins including antioxidant enzymes. Here we purified human cord blood glutathione reductase (hcbGR), glutathione S-transferase (hcbGST) and human cord blood glutathione peroxidase (hcbGPx) from human cord blood erythrocytes and analyzed the inhibition effects of the antibiotics incorporating cefuroxime, ceftriaxone, ceftizoxime and cefoperazone, on these enzymes. KI values for the drugs ranged from 10.42 to 28.72 M for hcbGR, 32.7 to 244.8 M for hcbGPx, and 32.39 to 267.3 M for hcbGST. Cefuroxime caused the highest inhibition on all enzymes with KI values of 10.42, 32.39, 32.7 M for hcbGR, hcbGST, and hcbGPx, respectively. All drugs displayed non-competitive inhibition regardless of their structures. Since these drugs are often used during pregnancy, identification of possible undesired impacts on various parameters has a great importance for pharmacological and medical applications.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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