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- ArticleAçık Erişim2023Favipiravir-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.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023ANTI-INFLAMMATORY, ANALGESIC, AND GASTRIC TISSUE EFFECTS OF LACIDIPINE, ASPIRIN, AND THEIR COMBINATION
Isik, Bahar; Ates, Irem; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Gulaboglu, Mine; Ozcicek, Adalet; Suleyman, Halis
The increase in cyclooxygenase-2 (COX-2) activity and the decrease in COX-1 activity were associated with increased intracellular calcium. Lacidipine, a calcium channel blocker, can protect gastric tissue from aspirin-induced damage while potentiating the analgesic and anti-inflammatory properties of aspirin. The aim of this study was to investigate the anti-inflammatory, analgesic, and gastric tissue effects of using lacidipine and aspirin in combination and separately. (LA). Twenty-four rats were randomly divided into CG (carrageenan control), LCG (carrageenan + lacidipine), ACG (carrageenan + aspirin), and LACG (carrageenan + LA) groups. Lacidipine 4 mg/kg, aspirin 100 mg/kg were given orally to the animals on an empty stomach. Carrageenan was injected into the hind paws of rats to induce inflammation and pain. Paw volumes were measured at 0, 1, and 4 hours after carrageenan administration, and paw pain thresholds were measured at 1 and 4 hours. After euthanasia (thiopental sodium, 50 mg/kg), paw and gastric tissues were excised and biochemically analyzed. Gastric tissues were also examined macroscopically. In the paw tissues of animals receiving lacidipine, malondialdehyde (MDA) was lower than in the CG and AG, while total glutathione (tGSH) was higher (p<0.05). Lacidipine inhibited COX-2, but not COX-1 isoenzyme. LA—lacidipine, and aspirin—inhibited inflammation and hyperalgesia at 1 and 4 hours, respectively. Lacidipine prevented aspirin-induced COX-1 inhibition and gastric ulcer formation. Lacidipine combined with aspirin may be beneficial for initiating its anti-inflammatory activity early, achieving a potent analgesic effect, and preventing aspirin-induced gastric injury.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023The 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.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2023Effect 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Effects of Mirtazapine on Liver Ischemia-Reperfusion Injury in Rats
Alemdar, Ali; Yilmaz, Ismayil; Ozcicek, Fatih; Bulut, Seval; Eden, Arif Onur; Gursul, Cebrail; Mendi, Ali Sefa; Kuzucu, Mehmet; Altuner, Durdu; Suleyman, Halis
Background and Objective: Ischemia-reperfusion (I/R) injury begins with tissue oxygen deprivation and continues with oxidative stress and inflammatory response. Mirtazapine is an antidepressant drug with antioxidant and anti-inflammatory properties. The current study was to investigate the effect of mirtazapine against I/R induced liver injury in rats. Materials and Methods: Albino Wistar-type male rats were divided into sham operation (SHAM), I/R (IR) and I/R+mirtazapine administrated (IRM) groups. One hour before anaesthesia, 20 mg kg(-1) mirtazapine was administered to the IRM group of the animals and distilled water was applied to the SHAM and IR groups as a solvent. I/R was achieved by clamping the hepatic artery (except for the SHAM group). Following I/R, all rat groups were killed with high-dose anaesthesia. Malondialdehyde (MDA), total glutathione (tGSH), nuclear factor kappa B (NF-kappa B), interleukin 1 beta (IL-1 beta) and tumour necrosis factor-alpha (TNF-alpha) were determined in liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were measured in blood serum. In addition, histopathological examination was performed on liver tissue samples. Results: Mirtazapine prevented increased levels of MDA, NF-kappa B, IL-1 beta, TNF-alpha, ALT and AST in liver tissue with I/R and a decrease in tGSH. Furthermore, mirtazapine has alleviated I/R-associated severe hepatocyte degeneration, necrosis and other structural disorders in the liver. Conclusion: Biochemical and histopathological experimental results suggest that mirtazapine may be useful in the treatment of I/R-induced liver injury.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Effect of 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Is Benidipine Effective in Preventing Gastric Ischemia/Reperfusion Injury?
Bilici, Sami; Tas, Hakan Gokalp; Mamedov, Renad; Suleyman, Bahadir; Kuyrukluyi, Ufuk; Yavuzer, Bulent; Bulut, Seval; Coban, Abdulkadir; Suleyman, Halis
Background and Objective: The preventive effect of benidipine on organs and tissues against oxidative and proinflammatory cytokine damage, whose production is elevated by I/R, has been demonstrated. The current study noted that benidipine affects the biochemical and histopathological effects of I/R therapy on gastric injury in rats. Materials and Methods: A total of 18 rats were divided into either a Sham operation group (SG), gastric ischemia/reperfusion (GIR) group or benidipine+gastric ischemia/reperfusion (BGIR) groups. Biochemical measures and histological exams were done in all three groups after I/R intervention. Results: The MDA, TNF-alpha, IL-1 beta and COX2 levels were significantly higher (p<0.001) in GIR compared to SG and BGIR, although tGSH and COX1 were significantly lower (p<0.001). The SG group was histopathologically normal. The surface epithelium broke off in spots, causing mild degeneration, the gland recesses were decreased, the gland neck areas were wide, the base areas were significantly oedematous and the blood capillaries showed moderate dilatation and congestion in the GIR group. Infiltration of polymorphonuclear cells was seen in the connective tissue surrounding the arteries and close to the gland bases. The BGIR group's histopathological results were not normal, although they were milder than the GIR group's. Conclusion: The results discovered that benidipine shifted the oxidant/antioxidant balance in I/R damage in favour of antioxidants, as well as the COX-1/COX-2 equilibrium in favour of COX-2, which is cytoprotective. It appears that administering benidipine for antioxidant and cytoprotective purposes before surgical operations that are likely to cause I/R damage may be advantageous.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Effect of tocilizumab on ischemia-reperfusion-induced oxido-inflammatory renal damage and dysfunction in rats
Erdem, Kezban Tuna Ozkaloglu; Bedir, Zehra; Kuyrukluyildiz, Ufuk; Tas, Hakan Gokalp; Suleyman, Zeynep; Bulut, Seval; Mendil, Ali Sefa; Sarigul, Cengiz; Unver, Edhem; Suleyman, Halis
Ischemia-reperfusion-induced (I/R) renal damage is a pathogenic process that starts with ischemia, then progresses through oxidative stress and inflammation. Tocilizumab (TCZ), a recombinant human monoclonal antibody produced against the IL-6 receptor, will be tested against renal I/R injury. TCZ is known to lower the levels of proinflammatory cytokines and oxidant mediators while raising the amounts of antioxidant molecules. Our purpose is to evaluate the biochemical and histological effects of TCZ against I/R-induced oxido-inflammatory kidney damage and dysfunction in rats. Animals were divided into 3 groups as renal I/R (RIR), I/R+ TCZ (IRT), and healthy group (HG). TCZ was administered at a dose of 8 mg/kg to the IRT group (n=6) of the animals, and distilled water as a solvent was administered intraperitoneally (ip) to the RIR (n=6) and HG (n=6) groups. Then, two hours of ischemia and six hours of reperfusion were applied to the left kidneys of IRT and RIR animals. TCZ significantly inhibited the increase in the levels of malondialdehyde (MDA), nuclear kappa B (NF-κB), tumour necrosis factor alpha (TNF-α), interleukin 1-β (IL-1β), IL-6, creatinine (Cr) and blood urea nitrogen (BUN) and decrease in total glutathione (tGSH) with I/R in renal tissue. TCZ also attenuated severe histopathological damage due to I/R in renal tissue. TCZ protected renal tissue from I/R-induced oxidative and inflammatory damage. These results indicate that TCZ may be useful in the treatment of renal I/R injury.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Effect of thymoquinone on cyclophosphamide-induced oxidative and inflammatory ovarian damage in rat
Colluoglu, Cagdas; Balci, Serdar; Gundogdu, Betul; Coban, Taha Abdulkadir; Bulut, Seval; Suleyman, Halis
This study intends to investigate the effect of thymoquinone against possible ovarian damage and infertility caused by cyclophosphamide in female rats. The rats in the experiment (n=36) were separated into three groups; cyclo-phosphamide administered, thymoquinone plus cyclophosphamide administered and healthy control. At the end of 30 days of administration, 6 rats from each group were killed and the biochemical and histopathological examina-tions were performed on the ovarian tissues. The remaining animals were kept in the same cage with mature male rats for two months. Infertility developed in 83% of cyclophosphamide group animals. Thymoquinone atte-nuated cyclophosphamide-related oxidative and inflammatory ovarian damage and reduced the development of infertility. The outcomes suggest that thymoquinone may be useful in treating infertility due to oxidative and inflammatory ovarian damage.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022EFFECT OF NIMESULIDE AGAINST INDOMETHACININDUCED OXIDATIVE LIVER DAMAGE IN RATS
Yilmaz, Canan T.U.Z.; Suleyman, Bahadir; Mammadov, Renad; Ozcicek, Adalet; Bulut, Seval; Yazici, Gulce N.A.Z.; Gulapoglu, Mine; Suleyman, Halis
Indomethacin is used in the treatment of ankylosing spondylitis, osteoarthritis, tendinitis, and other inflammations. However, it has been reported indomethacin has nephrotoxic, gastrotoxic, and hepatotoxic effects. The aim of this study is to investigate the effect of nimesulide on indomethacin-induced liver damage in rats biochemically and histopathologically. Experimental animals (21 rats) were divided into 3 groups: the healthy (HG) group receiving distilled water as a solvent, the 25 mg/kg indomethacin administered (IDO) group, and the 50 mg/kg nimesulide + 25 mg/kg indomethacin administered (NIDO) group. Malondialdehyde (MDA), total glutathione (GSH) levels and cyclooxygenase-1 (COX-1), cyclooxygenase (COX-2) enzyme activities were determined from liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were also measured in serum. The data obtained in the IDO group were compared with the data obtained from the NIDO and MDA and decreased tGSH levels with indomethacin HG groups. Increased application in liver tissue approached the HG group with nimesulide application, and the difference was found to be insignificant. Nimesulide prevented the decrease in COX-1 and COX-2 levels observed with indomethacin administration. Again, the increase in ALT and AST levels, which increased with indomethacin administration, was prevented by nimesulide. As a result of the histopathological evaluation, it was observed that nimesulide reduced the damage caused by indomethacin. Nimesulide at 50 mg/kg prevented oxidative liver damage induced with indomethacin at 25 mg/kg. Our results suggest that nimesulide may be useful in the treatment of hepatotoxicity and COX-1 inhibition side effects without suppressing analgesic and anti-inflammatory activity due to indomethacin use.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Effect 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.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Beneficial interaction of pycnogenol with indomethacin in rats
Ekinci, Bilge; Suleyman, Bahadir; Mammadov, Renad; Bulut, Seval; Ozcicek, Adalet; Ergul, Cetin; Gulaboglu, Mine; Hayme, Serhat; Suleyman, Halis
Cyclooxygenase 2 (COX-2) is responsible for the therapeutic effects of indomethacin, while inhibition of the COX-1 enzyme and oxidative stress are responsible for its gastro-toxic effects. It has been reported that pycnogenol increases the expression of COX-1, suppresses the expression rate of COX-2 and oxidative stress. Our aim in this study is to investigate the antiinflammatory activities of indomethacin, pycnogenol, and their combination (PI) in rats and to examine their effects on stomach tissue. In the study, anti-inflammatory activity was investigated in carrageenan-induced inflammatory paw edema in albino Wistar male rats. Effects on stomach tissue were performed by applying the previous method. PI, indomethacin and pycnogenol were the best suppressors of carrageenan inflammation and oxidative stress in paw tissue, respectively. While the groups with the lowest COX-1 activity in paw tissue were IC, PIC and PC, respectively, PIC, IC and PC were the ones that best inhibited the increase in COX-2 activity. Pycnogenol inhibited the increase of malondialdehyde, the decrease of total glutathione and COX-1 in the stomach, and significantly suppressed the formation of indomethacin ulcers. Our experimental results showed that pycnogenol reduced the toxic effect of indomethacin on the stomach and increased anti-inflammatory activity. This beneficial interaction of pycnogenol and indomethacin suggests that PI will provide superior success in the treatment of inflammatory diseases.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Effect 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Molecular 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022The Effect of Cerebrolysin on Ischemia Reperfusion-Induced Oxidative and Inflammatory Ovarian Damage in Rats
Ozer, Mehmet; Ince, Sefa; Suleyman, Bahadir; Mammadov, Renad; Yavuzer, Bulent; Bulut, Seval; Akbas, Nergis; Mokhtare, Behzad; Mendil, Ali S.; Dinc, Kemal
SUMMARY. Ovarian ischemia-reperfusion (I/R) injury develops due to oxidative stress and inflammation that occurs when tissue is deprived of oxygen. Ovarian I/R damage also causes infertility. The aim of this study is to see the effect of ovarian I/R damage on reproductive functions and to determine the protection of antioxidant and anti-inflammatory cerebrolysin in possible damage. Albino Wistar-type female rats were divided into sham operation (SG), ischemia-reperfusion (IR) and cerebrolysin+ischemia-reperfusion (CIR) groups. After I/R application with cerebrolysin, the ovaries of six animals from each group were taken and biochemical and histopathological examinations were performed. Six animals from each remaining group were left to breed. Our test results showed that cerebrolysin decreased I/R-related oxidant, proinflammatory cytokine and tissue damage and increased antioxidant levels. In addition, cerebrolysis significantly inhibited the delay of the maternity period. These findings indicate that cerebrolysin may be helpful in the treatment of I/R-related ovarian damage and infertility.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2022Effect of Rhodiola rosea Root Extract on Stress-Induced Gastric Ulcer in Rats
Isik, Bahar; Altuner, Durdu; Ozcicek, Fatih; Ezmeci, Talat; Aggul, Ahmet G.; Suleyman, Bahadir; Bulut, Seval; Suleyman, Zeynep; Yavuzer, Bulent; Suleyman, Halis
Stress can lead to stomach ulcers. Oxidative stress and inflammation are involved in the pathogenesis of stress ulcers. Rhodiola rosea root extract (RRE) has antistress, anxiolytic, antioxidant and anti-inflammatory effects. In this study, the effect of RRE on gastric ulcers induced by forced immobilization method (FIM) was investigated. Albino Wistar male rats were divided into healthy (HG), control (SC), stress+RRE (SRE) and stress+famotidine (SFM) groups. RRE was given to the rats’ SRE group, and famotidine to the SFM group was administered orally. One hour after, the animals in the SRE, SFM and SC groups were subjected to stress with FIM for one hour once a day. This procedure continued for seven days. After this period, the animals were euthanized. Stomach tissues were examined macroscopically and biochemically. RRE reduced the number and area of stress-induced ulcers and biochemical changes in the gastric tissues of animals better than famotidine.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Effect of taxifolin on cyclophosphamide-induced oxidative and inflammatory bladder injury in rats
Akbaş, Nergis; Suleyman, Bahadır; Mammadov, Renad; Yazıcı, Gülce Naz; Bulut, Seval; Süleyman, Halis
The role of oxidative stress and inflammation in the pathogenesis of cyclophosphamide-related side effects has been demonstrated in previous studies. This study aimed to investigate the effect of taxifolin, due to its antioxidant and anti-inflammatory properties, on cyclophosphamide-induced oxidative and inflammatory bladder injury in albino Wistar rats. The taxifolin+cyclophosphamide (TCYC) group was given 50 mg/kg of taxifolin orally by gavage. Normal saline was used as a solvent for the cyclophosphamide (CYC) group and the healthy control (HC) group. One hour after taxifolin administration, 75 mg/kg of cyclophosphamide was intraperitoneally injected in the TCYC and CYC groups. This procedure was repeated once a day for 30 days. At the end of this period, biochemical markers were studied in the excised bladder tissues and histopathological evaluations were conducted. In the histopathological evaluation of the CYC group, severe epithelial irregularity, dilatation, congestion, and polymorphonuclear leukocyte accumulation in the vascular structures were observed. Additionally, the malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) levels, the total oxidant status (TOS), and the oxidative stress index (OSI) values were significantly higher, and the total glutathione (tGSH) levels and total antioxidant status (TAS) were significantly lower in the CYC group in comparison to the HC group (P<0.001). Taxifolin reduced the cyclophosphamide-induced increases in the MDA, TNF-α, IL-1β, and IL-6 levels and the TOS and OSI values; it decreased the tGSH and TAS levels and reduced histopathological damage (P<0.001). Taxifolin may be useful in the treatment of cyclophosphamide-induced bladder damage.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022THE EFFECT OF CARVACROL UPON EXPERIMENTALLY INDUCED DIABETIC NEUROPATHY AND NEUROPATHIC PAIN IN RATS
Ekinci, Bilge; Suleyman, Bahadir; Mammadov, Renad; Gezer, Arzu; Mendil, Ali Sefa; Akbas, Nergis; Bulut, Seval; Dal, Cagatay Nusret; Suleyman, Halis
Diabetic neuropathies are the most frequent complication of diabetes. While numerous metabolic pathways are disrupted in diabetic neuropathy, oxidative stress has been indicated as a significant reason for this condition. In this study, the effect of carvacrol, which has antioxidant effects, on experimental diabetic neuropathy and neuropathic pain was investigated. Alloxan was used to induce diabetes in the experiment. Diabetes was created by administering 120 mg/kg of alloxan intraperitoneally (i.p) once a day for 3 days. Rats with a blood glucose concentration above 250 mg/kg in the blood taken from the tail veins at the end of three days were considered diabetic. Rats were categorized under healthy control (HG), alloxan-induced hyperglycemia (AG), and alloxan-induced hyperglycemia + carvacrol-treated (ACG) groups. Carvacrol was i.p injected at 50 mg/kg dose to the ACG (n = 6) group of rats with hyperglycemia. The same volume of distilled water as the solvent was applied in the same way to AG (n = 6) and HG (n = 6) rat groups. This procedure was repeated once a day for three months. Carvacrol showed an anti-hyperglycemic effect in diabetic rats, a protective effect against lowering pain threshold, and analgesic activity in rat paws. Carvacrol prevented the oxidant/antioxidant balance from changing in favor of oxidants. The results supported that carvacrol is an agent against alloxan-induced peripheral diabetic neuropathic pain.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022Effect of low and high dose of favipiravir on ovarian and reproductive function in female rats: Biochemical and histopathological evaluation
Balcı, Serdar; Çöllüoğlu, Çağdaş; Yavuzer, Bülent; Bulut, Seval; Altındağ, Fikret; Akbaş, Nergis; Süleyman, Halis
Favipiravir is a drug which shows antiviral activity by inhibiting RNA-dependent RNA polymerase. Favipiravir causes severe adverse effects at high doses. The aim of this study was to investigate the effects of low and high dose favipiravir on ovarian and reproductive function in female rats. The rats were divided into three groups: HG group (healthy rats), FAV-100 group (rats administered 100 mg/kg favipiravir), and FAV-400 group (rats administered 400 mg/kg favipiravir) with 12 rats in each group. Favipiravir was administered orally twice daily for 1 week. Six rats from each group were euthanized and their ovaries were removed. Oxidative and antioxidant parameters were measured in ovarian tissues and examined histopathologically. The remaining animals were kept to breed. Animals receiving favipiravir had increased oxidant content, decreased antioxidant activity, decreased histopathological damage, infertility, and gestational delay. Favipiravir treatment should be used with caution, especially in women of reproductive age.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2022The 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.
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