Sürdürülebilir Kalkınma Amaçları

  • ArticleYalnız künye2023
    Effect of Ketorolac and Nimesulide Combination on Surgical Pain, Stomach and Kidneys

    Isik, Bahar; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Yavuzer, Bulent; Altuner, Durdu; Gulaboglu, Mine; Suleyman, Halis

    Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID). Cyclooxygenase-2 (COX-2) inhibition from the therapeutic effects of NSAIDs and COX-1 inhibition from toxic effects are held responsible. It is known that nimesulide has formed a protective effect by inhibiting the decrease in COX-1 activity and the increase in COX-2 activity. In this study animals were divided into healthy (HG), paw-scalpel incision (PSI) control (PSIC), PSI+nimesulide (PSIN), PSI+ketorolac (PSIK), and PSI+nimesulide+ketorolac (PSI+NKC) administered groups. Nimesulide was administered orally(50 mg/kg), and ketorolac was administered intra-peritoneally(5 mg/kg). Nimesulide and ketorolac showed similar analgesia (p = 0.194), while NKC provided the best analgesia (p < 0.001). Nimesulide inhibited the increase of oxidant and COX-2 in gastric tissue and increased antioxidant and COX-1 levels, protecting the stomach tissue from ketorolac damage(p < 0.01). In addition, NKC reduced the area and number of ketorolac-induced gastric ulcers in the stomach (p<0.001). Nimesulide also prevented ketorolac-induced renal dysfunction (p < 0.001).

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  • ArticleAçık Erişim2023
    Favipiravir-induced inflammatory and hydropic degenerative liver injury in rats

    Bilici, Sami; Altuner, Durdu; Suleyman, Zeynep; Bulut, Seval; Sarigul, Cengiz; Gulaboglu, Mine; Altindag, Fikret; Ozcicek, Adalet; Gursul, Cebrail; Suleyman, Halis

    Background. Favipiravir is very effective in the treatment of many viral infections, especially at high doses. It was used at such doses to treat coronavirus disease 2019 (COVID-19) during the pandemic. However, liver damage was reported in patients undergoing such treatment. Objectives. This study aimed to investigate the effects of low and high doses of favipiravir on the liver of rats, using biochemical and histopathological methods. Materials and methods. Wistar albino rats were allocated to one of 3 groups, namely a healthy group (HG), a 100 mg/kg favipiravir (FAV-100) group and a 400 mg/kg favipiravir (FAV-400) group. Favipiravir was administered orally at 100 mg/kg and 400 mg/kg doses to the FAV-100 (n = 6) and FAV-400 (n = 6) groups, respectively. Distilled water was administered orally (1 mL) using the same method to the HG (n = 6). This procedure was repeated twice a day for 1 week. At the end of this period, the animals were euthanized with a high dose of thiopental anesthesia (50 mg/kg) and their liver tissues were removed. Results. Favipiravir caused an increase in malondialdehyde (MDA), nuclear factor kappa B (NF-κB) and interleukin 6 (IL-6) levels in the liver tissue, as well as elevated alanine aminotransaminase (ALT) and aspartate aminotransferase (AST) levels in the blood. Moreover, favipiravir caused a decrease in total glutathione (tGSH), superoxide dismutase (SOD) and catalase (CAT) levels. In addition, severe edema, lymphocyte infiltration and hydropic degeneration were observed in the liver tissue of the FAV-400. Conclusions. High-dose favipiravir caused more significant oxidative and inflammatory damage in the liver tissue of rats than low-dose favipiravir.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2023
    The Effect of Carvacrol on 5-Fluorouracil-Induced Optic Neuropathy in Rats. Histopathological and Biochemical Analysis

    Cicek, Ibrahim; Altuner, Durdu; Suleyman, Zeynep; Mammadov, Renad; Coban, Taha Abdulkadir; Gulaboglu, Mine; Yazici, Gulce Naz; Bayrakceken, Kemal; Suleyman, Halis

    5-Fluorouracil (5-FU) is also known to cause ocular toxicity. The purpose of this study was to investigate the effects of Carvacrol upon possible 5-FU-induced optic nerve damage in rats biochemically and histopathologically. In this study totally, eighteen albino Wistar male rats were used. The rats were grouped under three categories as the healthy (HG) (n=6), 100 mg/kg 5-FU treated alone (FUG) (n=6) and 50 mg/ kg Carvacrol+100 mg/kg 5-FU (CFU) groups (n=6). Carvacrol at 50 mg/kg was injected intraperitoneally (ip) to the CFU group. The same volume of 0.9% NaCl was administered as the solvent ip to HG and FUG groups. One hour after administrating Carvacrol and solvent, 100 mg/kg 5-FU was ip injected to CFU and FUG groups. Carvacrol was administered once daily for 10 days. Three-dose 5-FU was administered on the 1st, 3rd, and 5th days as one dose each. On the 10th day, the animals were euthanised with high-dose anesthesia and optic nerve tissues were removed. Malondialdehyde (MDA), reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), and Interleukin (IL-6) levels were measured in optic nerve tissues. The tissues were also examined histopathologically. The results obtained from HG and CFU groups were compared with the FUG group. Significantly higher MDA and IL-6 levels (p < 0.001) and significantly lower (p < 0.001) tGSH, SOD, and CAT levels were determined in optic nerve samples of the FUG group rather than HG and CFU groups. In histopathological analyses, determined that astrocyte and oligodendrocyte nuclei were mostly darkly stained, the majority of astrocytes were hypertrophied and degenerated, and some oligodendrocytes were degenerated in the FUG group unlike HG and CFU groups. Moreover, the optic nerve tissue was determined to be vacuolized and intensely edematous, and blood capillaries were intensely dilated and congested. In conclusion, 5-FU caused optic neuropathy due to oxidative and inflammatory damage, and Carvacrol reduced this oxidative and inflammatory damage and histopathological changes in tissues. This revealed that Carvacrol was possibly to be efficient upon 5-FU-induced optic nerve toxicity.

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  • ArticleAçık Erişim2023
    The effects of sugammadex on gastric ischemia-reperfusion injury in rats: Biochemical and histopathological evaluation

    Koç, Alparslan; Kuyrukluyildiz, Ufuk; Gazi, Mustafa; Sayar, Ali Caner; Altuner, Durdu; Süleyman, Halis; Yavuzer, Bülent; Çoban, Taha Abdulkadir; Süleyman, Zeynep; Yazici, Gülce Naz

    The primary sources of reactive oxygen species (ROS) that cause ischemia-reperfusion (I/R) injuries are enzymes xanthine oxidase (XO) and nicotinamide adenine dinucleotide phosphate oxidases (NOXs) in the literature, whereby one of the main ROS producing cells via NOX activity are polymophonuclear leukocytes (PNL). Sugammadex, the effect of which we plan to research against gastric I/R damage, is a modified gamma-cyclodextrin that antagonizes the action of steroidal neuromuscular blocking drugs. Previous studies have reported that sugammadex inhibits PNL infiltration. However, it is unknown whether an inhibitory effect on XO is present. We aimed to biochemically and histopathologically investigate the effects of sugammadex on I/R-induced stomach damage in rats. The animals were divided into groups that underwent gastric ischemia-reperfusion (GIR), 4 mg/kg sugammadex + gastric ischemia-reperfusion (SGIR), and a sham operation group (SG). The effect of sugammadex was evaluated by measuring oxidant-antioxidant and PNL parameters. There was no significant difference in XO levels between the SGIR and GIR groups. In the SGIR group, sugammadex inhibited the increase in myeloperoxidase (MPO) and malondialdehyde (MDA) levels (p < 0.001). The amount of MDA and MPO in the SGIR group was similar as in the SG group. Sugammadex significantly suppressed the decrease in tGSH levels in the SGIR group (p < 0.001). The difference between tGSH levels in the SG and SGIR groups was slight. In the SGIR group, sugammadex significantly suppressed the increase in tumor necrosis factor alpha (TNF-α) and interleukin 1 beta (IL1-β) levels compared to the GIR group (p < 0.001). Additionally, sugammadex corrected histopathological modifications as much as sham group. In conclusion, sugammadex may be beneficial in preventing oxidative stress.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2023
    The Role of Adrenaline, Noradrenaline, and Cortisol in the Pathogenesis of the Analgesic Potency, Duration, and Neurotoxic Effect of Meperidine

    Yilmaz, Mehmet; Suleyman, Bahadir; Mammadov, Renad; Altuner, Durdu; Bulut, Seval; Suleyman, Halis

    Background and Objectives: The purpose of the study was to investigate the role of adrenaline (ADR), noradrenaline (NDR), and cortisol in the pathogenesis of the analgesic potency, duration, and epilepsy-like toxic effect of meperidine. Materials and Methods: The experimental animals were separated into 11 groups of six rats. In the meperidine (MPD) and metyrosine + meperidine (MMPD) groups, paw pain thresholds were measured before and after the treatment between the first and sixth hours (one hour apart). In addition, ADR and NDR analyses were performed before and after the treatment, between the first and fourth hours (one hour apart). For the epilepsy experiment, caffeine, caffeine + meperidine, and caffeine + meperidine + metyrapone groups were created, and the treatment was applied for 1 day or 7 days. Groups were created in which caffeine was used at both 150 mg/kg and 300 mg/kg. Epileptic seizures were observed in epilepsy groups, latent periods were determined, and serum cortisol levels were measured. Results: In the MPD group, pain thresholds increased only at the first and second hours compared to pre-treatment, while ADR increased at the third hour, leading to a decrease in pain thresholds. In the MMPD group, the increase in paw pain thresholds at 1 and 6 h was accompanied by a decrease in ADR and NDR. In the caffeine (150 mg/kg) + meperidine group, 1-day treatment did not cause epileptic seizures, while seizures were observed and cortisol levels increased in the group in which treatment continued for 7 days. When cortisol levels were compared between the group in which caffeine (300 mg/kg) + meperidine + metyrapone was used for 7 days and the animals receiving caffeine (300 mg/kg) + metyrapone for 7 days, it was found that cortisol levels decreased and the latent period decreased. Conclusions: The current study showed that if serum ADR and cortisol levels are kept at normal levels, a longer-lasting and stronger analgesic effect can be achieved with meperidine, and epileptic seizures can be prevented.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2023
    Effect of pycnogenol on ischemia/reperfusion-induced oxidative and inflammatory damage intheovariesof rats

    Dinc, Kemal; Kiremitli, Sevil; Suleyman, Bahadir; Mammadov, Renad; Yavuzer, Bulent; Bulut, Seval; Yazici, Gulce N.; Coban, Taha A.; Altuner, Durdu; Suleyman, Halis

    Purpose: To investigate the protective effect of pycnogenol (PYC) against ischemia/reperfusion (I/R) ovarian damage induced by experimental ovarian torsion in rats using biochemical and histopathological methods. Methods: Four groups of rats (n = 6) were randomly assigned and designated as follows - SG: sham group, PCG: pycnogenol (40 mg/kg) group, IRG: ovarian ischemia-reperfusion group, and PIR: pycnogenol (40 mg/kg) + ovarian ischemia-reperfusion group. In IRG and PYC treatment groups, ischemia was induced in the right ovary for two hours with vascular clips. The ovary was reperfused for two hours after ischemia was induced. Then, the levels of malondialdehyde (MDA), total glutathione (tGSH), nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) in the ovarian tissues of rats were examined. Ovarian tissues were also examined histopathologically and follicle counts were performed. Results: Histopathological examination revealed that the developing follicles in ovary of I/R-induced group showed both morphological and cellular degeneration and vascular pathology. The PYC treatment group showed less ovarian damage, edema and vascular pathology than I/R-induced group (p < 0.05). The MDA, NF-κB, TNF-α and IL-1β levels in I/R-induced group were significantly higher than in SG and tGSH levels were significantly reduced by I/R damage (p < 0.05). Pycnogenol treatment reversed these biochemical indices as well as I/R-induced histopathological changes. Conclusion: Pycnogenol has a protective effect in rat ovaries by alleviating I/R-induced changes in biochemical parameters and histological disruptions. Further studies, including those in humans, to determine the effect of PYC on ovarian injuries would be required.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2022
    Effects 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.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2022
    Effect of Thymoquinone on Diclofenac-Induced Liver Injury

    Ekinci, Bilge; Altuner, Durdu; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Suleyman, Zeynep; Gul, Mehmet A.; Ergul, Cetin; Suleyman, Halis

    Background and Objective: Thymoquinone (TQ) is an active phenolic compound obtained from Nigella sativa L. It has anti-inflammatory and antioxidant activity by inhibiting the overproduction of certain inflammatory molecules and lipid peroxidation. TQ also has a hepatoprotective effect. This study, it was aimed to biochemically investigate the effect of TQ on diclofenac (DC)-induced liver damage in rats. Materials and Methods: The animals were divided into healthy control (HG), only diclofenac (DG), only thymoquinone (TQG) and diclofenac+thymoquinone (DTQG) groups. The DC was injected intraperitoneally at a dose of 25 mg kg(-1). The TQ was administered orally to the stomach at a dose of 20 mg kg(-1). This procedure was repeated once a day for 7 days. Results: Biochemical test results showed that TQ significantly prevented the increase in oxidant parameters and the decrease in antioxidants in liver tissue, which is formed by DC. Also, DC and TQ inhibited the increase of proinflammatory cytokines in liver tissue. The TQ also prevented the decrease of COX-1 activity by DC and increased the inhibition of COX-2. The TQ also significantly suppressed the elevation of liver function markers such as Alanine Aminotransferase (ALT) and Aspartate Aminotransferase (AST) with DC. Conclusion: These findings indicated that the hepatotoxic effect of DC was due to oxidative stress and inhibition of cytoprotective structural COX-1 enzyme. It suggested that TQ may be useful in the treatment of DC-related liver injury.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2022
    Effect of Thymoquinone on Everolimus-Induced Oral Toxicity in Rats. A Macroscobic and Biochemical Evaluation

    Dilber, Muhammet; Salcan, Ismail; Suleyman, Bahadir; Mammadov, Renad; Altuner, Durdu; Aggul, Ahmet G.; Esen, Mehtap; Bulut, Seval; Suleyman, Zeynep; Yavuzer, Bulent

    Everolimus is a drug within the class of mammalian target of rapamycin inhibitors (mTOR). The most widespread side effect observed is oral mucositis.Thymoquinone is a phenolic compound obtained antioxidant and anti-inflammatory activities. The aim of this study is to investigate the protective effect of thymoquinone against oral toxicity that may develop due to everolimus in rats. Albino Wistar male rats were divided into healthy(HG), everolimus(EVR), thymoquinone(TQG) and thymoquinone+everolimus(TQE) groups. Thymoquinone (20 mg/kg) was administered to the TQG and TQE groups orally. One h after, TQE and EVR groups were given everolimus to (2 mg/kg) the stomach. This procedure was repeated once a day for four weeks. After 4 weeks, animals were euthanized, tongue and cheek tissues were examined biochemically and histopathologically. Thymoquinone prevented the increase of oxidant and proinflammatory cytokines and the decrease of antioxidants in the tongue and cheek tissues of animals, and also reduced the histopathological damage.

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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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  • ArticleYalnız künye2022
    Effect 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.

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  • ArticleAçık Erişim2022
    The effects of taxifolin on neuropathy related with hyperglycemia and neuropathic pain in rats: A biochemical and histopathological evaluation

    Alay, Murat; Sonmez, Miyase Gulcin; Sakin, Aysegul; Atmaca, Murat; Suleyman, Halis; Yazici, Gulce Naz; Coban, Abdulkadir; Suleyman, Bahadir; Bulut, Seval; Altuner, Durdu

    Background. Hyperglycemia can be considered a determining factor in the development of diabetic neuropathy as well as neuropathic pain. There is a relationship between the excessive production of reactive oxygen species (ROS) and the pathogenesis of diabetic neuropathic pain. Taxifolin, on the other hand, is a flavonoid that has been documented to inhibit ROS production. Objectives. To investigate the effects of taxifolin, which has antioxidant and neuroprotective effects, on alloxan-induced hyperglycemia-induced neuropathy and neuropathic pain, biochemically and histopathologically. Materials and methods. The albino Wistar male rats were divided into 3 groups: Healthy group (HG), only alloxan group (AXG) and alloxan+taxifolin group (ATG). Hyperglycemia in animals was caused through intraperitoneal injection of alloxan at a dose of 120 mg/kg. Paw pain thresholds of animals were measured using Basile algesimeter. Sciatic nerve tissues were examined biochemically and histopathologically in order to evaluate neuropathy. Results. Our experimental results revealed that taxifolin significantly prevented the increase of plasma glucose concentration level with alloxan administration, the decrease of the paw pain threshold related to hyperglycemia, the change of oxidant-antioxidant balance in the sciatic nerve tissue in favor of oxidants, and the deterioration of tissue morphology in animals. Conclusions. Our experimental results indicate that taxifolin alleviates alloxan-induced hyperglycemia-related neuropathy and neuropathic pain.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2021
    Usnea Longissima Ekstresinin Akciğer Kanseri Hücre Kültürüne (A549) Etkisi

    Eksi, Saliha; Altuner, Durdu; Suleyman, Halis; Turumtay, Emine Akyuz

    Amaç: Bazı likenlerin antikanser aktivitesi olduğu bilinmektedir. Ancak, Usnea longisima liken türünün insan akciğer kanser \rhücrelerine (A549) karşı aktivitesine ait bilgilere rastlanmadı. Bu \rçalışmanın amacı Usnea longisima’nın, A549 hücre hattına etkisini araştırmaktır.\rGereç ve Yöntem: Usnea longisima ekstresinin kültür ortamında A549 hücre morfolojisine etkisi 400 µg/ml konsantrasyonda araştırıldı ve Olympus inverted mikroskobu (CK x 41, 10 x) ile \rincelendi. Usnea longisima ekstresinin sitotoksik aktivitesi 400, \r200, 100, 50, 25, 12.5 ve 6,75 µg/ml kosantrasyonlarda 1983’te \rMosmann tarafından yayınlanan protokole göre test edildi.\rBulgular: DMSO A549 hücre hattı üzerinde toksik etki oluşturmamıştır. Ancak, Usnea longisima ekstresi uygulanan A549 \rhücrelerin tamamına yakını ölmüştür. Ayrıca, Usnea longisima \rekstresinin hücreleri yüzeyden kopararak ölümüne neden olduğu anlaşılmaktadır.\rSonuç: Usnea longisima ekstresi, in vitro ortamda A549 kanser \rhücreleri üzerinde doza bağlı olarak sitotoksik etki oluşturmuştur. Bu nedenle akciğer kanserlerinin tedavisinde faydalı olabileceği düşünülmektedir.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2021
    Effect of adenosine triphosphate, benidipine and their combinations on bevacizumab-induced kidney damage in rats

    Kocaturk, Hüseyin; Bedir, Fevzi; Turangezli, Ömer; Arslan, Remzi; Çoban, Taha Abdulkadir; Altuner, Durdu; Suleyman, Halis

    Background. Bevacizumab-induced vascular endothelial growth factor (VEGF) inhibition may lead to a decrease in adenosine triphosphate (ATP) levels, an increase in intracellular Na+ and Ca2+ concentrations and an increase in reactive oxygen species (ROS) generation, as well as to cell damage. Objectives. To investigate the biochemical and histopathological effects of ATP, benidipine and ATP in combination with benidipine on bevacizumab-induced kidney damage in rats. Materials and methods. Rats were divided into 5 treatment groups: bevacizumab (BVZ) alone, ATP + bevacizumab (ABVZ), benidipine + bevacizumab (BBVZ), ATP + benidipine + bevacizumab (ABBVZ), and healthy controls (HC). Adenosine triphosphate (25 mg/kg), benidipine (4 mg/kg orally), ATP (25 mg/kg) + benidipine (4 mg/kg), or saline were administered to albino Wistar rats. One hour after treatment, bevacizumab was injected at a dose of 10 mg/kg to induce kidney damage. Two doses of bevacizumab were delivered 15 days apart. Adenosine triphosphate + benidipine were administered once a day for 1 month. Results. Malondialdehyde (MDA), total oxidant status (TOS), creatinine, and blood urea nitrogen (BUN) levels of the BVZ, BBVZ, ABVZ, ABBVZ, and HC groups were ranked from highest to lowest. Conversely, total glutathione (tGSH) and total antioxidant status (TAS) kidney tissue values were ranked from lowest to highest, respectively. Hemorrhage, tubular necrosis and grade 3 focal tubular atrophy were observed in the BVZ group. Atrophy and grade 2 necrosis were observed in the BBVZ group and atrophy and grade 1 necrosis were observed in the ABVZ group. Only grade 1 atrophy was observed in the ABBVZ group. Conclusions. Adenosine triphosphate reduced bevacizumab-induced renal toxicity significantly more effectively than benidipine. However, the combination of ATP + benidipine further reduced bevacizumab-induced renal toxicity relative to benidipine or ATP alone. These data indicate that ATP + benidipine might be a potential therapeutic strategy for the prevention of bevacizumab-induced renal toxicity.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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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
    Effect of Taxifolin on Ischemia/Reperfusion-Induced Oxidative Injury of Sciatic Nerve in Rats

    Yuceli, Sahin; Suleyman, Bahadir; Yazici, Gulce Naz; Mammadov, Renad; Cankaya, Murat; Kunak, Celaleddin Semih; Bulut, Seval; Suleyman, Halis; Altuner, Durdu

    Background: Ischemia is a condition in which blood flow to tissues is decreased or entirely stopped for various reasons. The reperfusion process exacerbates damage caused by ischemia in the organs and tissues. Reactive oxygen species (ROS) are mainly responsible for ischemia-reperfusion (IR) damage. ROS increase results in lipid peroxidation (LPO) and oxidative stress. In the literature, taxifolin reportedly suppresses ROS production. This study aimed to determine the effect of taxifolin, which is a flavonoid, on IR injury of the sciatic nerve in rats. Methods: This study divided 30 albino Wistar rats into 3 groups: IR without medication (IR) group, taxifolin applied IR (TAX+IR) group, and only dissection made to the sciatic nerve sham group (SHAM). Sciatic nerve injury was induced by applying 2 hours of ischemia and 3 hours of reperfusion to the abdominal aorta and iliolumbar arteries. Biochemical and histopathologic investigations then were performed on sciatic nerve tissues. Malondialdehyde, total glutathione, glutathione reductase, and glutathione peroxidase were analyzed as oxidative stress markers, and tumor necrosis factor–α and interleukin-1β levels were evaluated as inflammatory stress markers in biochemical tests. Results: The IR group has statistically significantly high oxidant and cytokine levels and low antioxidant levels compared with the TAX+IR group. Taxifolin treatment was also shown to cause significant histopathologic improvement. Conclusions: We suggest that taxifolin may be effective in preventing IR injury of the sciatic nerve.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2021
    Protective effect of taxifolin against prooxidant and proinflammatory kidney damage associated with acrylamide in rats

    Bedir, Fevzi; Kocatürk, Hüseyin; Yapanoğlu, Turgut; Gürsul, Cebrail; Arslan, Remzi; Mammadov, Renad; Çoban, Abdülkadir; Altuner, Durdu; Suleyman, Halis

    The current study investigates the biochemical and histopathological effects of taxifolin on acrylamide-induced kidney damage. A 50 mg/kg dose of taxifolin was administered via oral gavage to the taxifolin + acrylamide (TACR) group (n-6) consisting of male albino Wistar rats. The same volume of distilled water used as solvent was orally administered to the acrylamide (ACR) (n-6) and healthy (HG) (n-6) groups. One hour after the administration of taxifolin and distilled water, a 20 mg/kg dose of acrylamide was orally administered to the TACR and ACR groups. This procedure was repeated once a day for 30 days. In the acrylamide group, malondialdehyde (MDA), tumour necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) levels were found to be high, total glutathione (tGSH) levels were found to be low, and there was severe interstitial haemorrhage; additionally, tubular necrosis, tubular atrophy, leucocyte infiltration, and glomerular structures with expanded Bowman's space were observed. In the taxifolin group, where the increase of MDA, IL-1β, and TNF-α and the decrease of tGSH associated with acrylamide have been prevented, any histopathological finding other than mild necrosis and atrophic tubules was not found. This suggests that Taxifolin would prevent kidney tissue from acrylamide-induced damage would be effective in treating acrylamide-induced nephrotoxicity, inhibiting the increase of MDA, IL-1β and TNF-α, and decreasing tGSH associated with acrylamide.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleAçık Erişim2021
    Effect of Sunitinib on Liver Oxidative and Proinflammatory Damage Induced by Ischemia-Reperfusion in Rats

    Bilici, Sami; Yazici, Gulce Naz; Altuner, Durdu; Aggul, Ahmet Gokhan; Suleyman, Halis

    Background: Ischemia-reperfusion (IR) injury is defined as a complex pathologic process that begins with the oxygen deprivation of tissue, continues with the production of reactive oxygen radicals (ROS), and expands with an inflammatory response. This study investigates the protective effects of sunitinib, an anticancer drug with demonstrated antioxidant and anti-inflammatory activity, against liver IR damage. Our study aims to investigate the biochemical and histopathologic effects of sunitinib on IR-induced liver damage in rats. Methods: Albino Wistar male rats were divided into 3 groups: liver IR control (IR), 25 mg/kg sunitinib + liver IR (S+IR), and sham operation (SHAM). Results: In the liver tissue of the IR group, oxidant and proinflammatory cytokine levels such as malondialdehyde, nuclear factor κ B, tumor necrosis factor-α, and interleukin-1β increased compared with the SHAM and S+IR groups. In addition, antioxidant levels such as total glutathione, glutathione reductase, and glutathione peroxidase were found to be significantly lower in the IR group than in the SHAM and S+IR groups. Although severe histopathologic damage was observed in the IR group, it was evaluated as mild in the S+IR group. The results obtained suggest that sunitinib may be helpful in the treatment of liver IR injury.

    • SDG 3 · Sağlık ve Kaliteli Yaşam
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  • ArticleYalnız künye2021
    Effect of rutin on methotrexate-induced oxidative lung injury in rats: A biochemical and histopathological evaluation

    Unver, Edhem; Olmez, Hasan; Tosun, Mustafa; Bilgin, Asli Ozbek; Ozcicek, Adalet; Aktas, Mehmet; Cimen, Ferda Keskin; Altuner, Durdu; Suleyman, Halis

    Methotrexate (MTX) is a chemotherapeutic drug that is frequently used in the treatment of cancer. However, pulmonary toxicity is one of its serious life-threatening side effects. Our study aims to investigate the effect of rutin on MTX-induced pulmonary toxicity in rats biochemically and histopathologically. The experiment was performed on 18 albino Wistar rats, including the healthy group (C), MTX group (MTX), and MTX + routine group (MTX+R). As a result, rutin suppressed the increase of MDA and the decrease of tGSH with MTX administration. Rutin significantly decreased the amount of TNF-α, while NF-κB increased with MTX. Rutin also reduced the histopathological findings, such as severe chronic inflammatory cell infiltration in the peribronchial and perivascular areas, bronchial dilatation, pulmonary artery vessel wall thickening, pulmonary artery dilation, and congestion. Rutin attenuated MTXinduced oxidative and inflammatory lung injury. These findings indicate that rutin may be useful in the treatment of MTX-related lung injury.

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