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- ArticleYalnız künye2021Molecular Mechanism of the Protective Effect of Tianeptine Against Ketamine-Induced Cardiac Injury in Rats
Yildiz, Sevler; Ugur, Kerim; Tas, Hakan G.; Ozcicek, Fatih; Kuyrukluyildiz, Ufuk; Mendil, Ali S.; Cankaya, Murat; Mamedov, Renad; Suleyman, Halis
Ketamine is a short-acting anesthetic drug that is derived from phencyclidine. Ketamine is used to treat depression and chronic pain disorders, as well as for anesthesia, analgesia, and sedation. Ketamine’s sympathomimetic characteristic causes cardiotoxicity. The pathophysiology of ketamine’s harmful impact has been linked to reactive oxygen species (ROS) and proinflammatory cytokines such as interleukin 1 beta (IL-1), interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-α). Tianeptine is an antidepressant that works similarly to tricyclic antidepressants. According to studies, tianeptine reduces the production of proinflammatory cytokines such as ROS, IL-1, IL-6, and TNF-α. Tianeptine has a sympatholytic action as well. All of this evidence suggests that tianeptine might help to reduce ketamine cardiotoxicity. The goal of our research is to use biochemical and histological techniques to see how tianeptine affects ketamine-induced cardiotoxicity in rats.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021The effect of dexmedetomidine on gastric ischemia reperfusion injury in rats. Biochemical and histopathological evaluation
Kuyrukluyildiz, Ufuk; Delen, Leman Acun; Onk, Didem; Yazici, Gulce Naz; Gulaboglu, Mine; Suleyman, Halis
Purpose: To evaluate the protective effect of dexmedetomidine on gastric injury induced by ischemia reperfusion (I/R) in rats. Methods: A total of 18 male albino Wistar rats were divided groups as: gastric ischemia reperfusion (GIR), gastric ischemia reperfusion and 50 μg/kg dexmedetomidine (DGIR) and sham operation (HG) group. After the third hour of reperfusion, the biochemical and histopathological examinations were performed on the removed stomach tissue. Results: Malondialdehyde (MDA) and myeloperoxidase (MPO) levels were found to be significantly higher in GIR compared to HG (p < 0.05). A statistically significant decrease was observed at the DGIR compared to the GIR for oxidants levels. Total glutathione (tGSH) and superoxide dismutase (SOD) levels were statistically significantly decreased at the GIR, and antioxidants levels were found to be significantly higher in the DGIR (p < 0.05) There was no significant difference between HG and DGIR in terms of SOD (p = 0.097). The DGIRs’ epitheliums, glands and vascular structures were close to normal histological formation. Conclusions: Dexmedetomidine is found to prevent oxidative damage on the stomach by increasing the antioxidant effect. These results indicate that dexmedetomidine may be useful in the treatment of ischemia-reperfusion-related gastric damage.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021Effects of Benidipine Hydrochloride on Ischemia Reperfusion Injury of Rat Brain
Cakir, Tayfun; Yucetas, Seyho Cem; Yazici, Gulce Naz; Sunar, Mukadder; Arslan, Yusuf Kemal; Suleyman, Halis
AIM: To evaluate the neuroprotective effects of benidipine hydrochloride on the cerebral cortex tissues in rats exposed to cerebral ischemia-reperfusion (I/R) injury. MATERIAL and METHODS: Twenty-four male Wistar albino rats were randomly divided into three groups, and administered benidipine hydrochloride (10 µg/kg/day) orally through a catheter for 2 h to form the study group (BIR group, n=8). The I/R procedure was performed in the rats of the IR group (n=8), and a sham group was formed to determine the normal structure of the cerebral cortex (n=8). Transient ischemia was performed by clamping the left common carotid artery for 2 h. Subsequently, reperfusion was applied for 12 h. Cerebral infarct volumes were measured and cerebral cortex tissue samples were analyzed histopathologically and biochemically by measuring malondialdehyde (MDA), total glutathione, cyclooxygenase 1 (COX-1), COX-2 and superoxide dismutase (SOD) RESULTS: The infarct area was markedly reduced in the BIR group vs. the IR group. Histopathologically, neuroprotective effects of benidipine hydrochloride were observed in the cerebral cortex tissues. The mean malondialdehyde and COX-2 levels were statistically higher in the IR group; however, in the BIR group, these levels were within the normal limits. Furthermore, the mean total glutathione, COX-1 and SOD levels were markedly lower in the IR group, and within the normal limits in the BIR group. CONCLUSION: Benidipine hydrochloride may play a certain protective role in cerebral I/R injury. This effect may be related to improvement in the antioxidant capacity of brain tissue, and the inhibition of overproduction of inflammatory cytokines.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021Effect 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Valeriana 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Effect of diazepam, sertraline and melatonin on the stress-induced reproductive disorders and intrauterine growth restriction in female rats
Aynaoglu Yildiz, Gulsah; Yildiz, Duran; Yapca, Omer Erkan; Suleyman, Bahadir; Arslan, Yusuf Kemal; Kurt, Nezahat; Suleyman, Halis
Objective: Psychological stress is an important factor triggering depression and anxiety. Infertility is known to cause stress; however, it is not clearly known whether stress causes infertility as well. In addition, there are different opinions accounting for the relation of stress-induced oxidative stress to infertility and intrauterine growth restriction. The aim of the study is to examine the effect of sertraline, diazepam and melatonin on the infertility, intrauterine growth restriction and oxidative stress that can be caused by forced immobilization stress management (FISM) in female rats. Materials and methods: Wistar rats were grouped as healthy rats (HG) applied distilled water, stress treated control group (SC), and 20 mg/kg sertraline + stress (SS), 2 mg/kg diazepam + stress (DS) and 10 mg/kg melatonin + stress (MS) treated rats. The medicines were administered orally once a day for 30 days. At the end of this period, oxidant/antioxidant parameters were measured through the blood samples collected from the tail veins of all rats. Then the rats were kept in a suitable environment for 2 months for breeding. Results: FISM caused oxidative stress in blood serum of animals, infertility and intrauterine growth restriction (decrease in birth weight of the baby). Best medicines to suppress FISM-related oxidative stress are melatonin > diazepam > sertraline respectively, while sertraline > diazepam > melatonin were most successful in terms of preventing infertility. The best medicines preventing the FISM-caused intrauterine growth restriction were found to be melatonin > diazepam > sertraline, respectively. Conclusion: FISM causes oxidative stress in animals. Oxidative stress is understood to affect the intrauterine growth negatively although it is not a major component in the pathogenesis of infertility. While melatonin is only effective in preventing the oxidative stress-related intrauterine growth restriction, antidepressants and anxiolytic treatment were found to be helpful in preventing both infertility and intrauterine growth restriction.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021The effect of lutein on ischemia-reperfusion-induced vasculitic neuropathic pain and neuropathy in rats
Yuceli, Sahin; Yazici, Gulce Naz; Mammadov, Renad; Suleyman, Halis; Ozdogan, Selcuk
Background/Aim: Neuropathic pain and neuropathy is commonly seen after ischemia-reperfusion injuries. Our aim was to evaluate the effect of lutein on ischemia-reperfusion (I/R)- induced vasculitic neuropathic pain and neuropathy in rats. Materials and Methods: An hour before anesthesia, 6 Albino Wistar male rats with I/R were orally administered with 1 mg/kg lutein (LIR group). Two groups of 6 such rats who underwent surgery were provided with 0.5 ml distilled water (as solvent) either via oral administration (SIR group) or by gavage (sham group or SG). One hour following the administration, the later femoral arteries of the LIR and SIR rats were closed using a sterile silk thread and ischemia was induced in the sciatic nerve for 4 h, followed by reperfusion for 24 h. The femoral artery of the SG group was not closed with suture. Next, 1 mg/kg lutein was re-administered only to the LIR group for 1 h, followed by measurement of the paw pain thresholds by the Basile Algesimeter. The levels of malondialdehyde (MDA), total glutathione (tGSH), nuclear factor-kB (NF-κB), and tumor necrosis factor-alpha (TNF-α) in the sciatic nerve tissues were measured, and the tissues were histopathologically examined. Results: We found that the MDA, NF-κB, and TNF-α levels were higher and the tGSH level was lower in the SIR group relative to those in the LIR group, and the differences were statistically significant. Significant histopathological damage was noted in the SIR group, whereas the LIR group demonstrated protection from oxidative damage. Conclusion: Lutein is potentially useful in the treatment of I/R-related neuropathy and neuropathic pain.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021Oxidative and pro-inflammatory lung injury induced by desflurane inhalation in rats and the protective effect of rutin
Tosun, Mustafa; Olmez, Hasan; Unver, Edhem; Arslan, Yusuf Kemal; Cimen, Ferda Keskin; Ozcicek, Adalet; Aktas, Mehmet; Suleyman, Halis
Background. Desflurane is a mainstay of general inhaled anesthetics with a methyl ethyl ether structure and is widely used in clinical practice. It has been reported to induce inflammation and lipid peroxidation in rat pulmonary parenchyma, to increase alveolar macrophages, and to cause peribronchial infiltration and edema. Rutin, a flavonoid vitamin P1, is known to have biological properties including acting as an antioxidant, an anti-inflammatory, and an inhibitor of bronchoalveolar polymorphonuclear leukocyte (PNL) infiltration. Objectives. The aim of this study is to examine the effects of rutin on desflurane-induced pulmonary injury using biochemical and histopathological methods. Materials and methods. The rats were divided into 3 groups (n = 6 each): healthy control (HC), rutin+desflurane-treated (DRT) and desflurane-only (DSF). Briefly, 50 mg/kg of rutin was given orally to the DRT group and an equal volume of normal saline was given to the DSF and HC groups. After 1 h, anesthesia was induced and maintained in the DRT and DSF groups for 2 h. After the rats had been sacrificed, the lungs were removed. Malondialdehyde (MDA), total glutathione (GSH), tumor necrosis factor alpha (TNF-α), and nuclear factor kappa B (NF-κB) levels were measured in the excised lung tissue. The removed tissues were also fixed in 10% formalin, and the obtained sections were stained with hematoxylin and eosin (H&E) and evaluated under light microscopy. The biochemical and histopathological results of the DRT group were compared with those obtained from the DSF and HC groups. Results. Desflurane increased MDA, TNF-α and NF-κB, and decreased GSH in lung tissue. The PNL infiltration, alveolar macrophages, hemorrhage, alveolar damage, and edema were observed in the lung tissue of the DSF group. Rutin was histopathologically shown to protect lung tissue from oxidative stress by preventing an increase in oxidant parameters and a decrease in antioxidants. Conclusions. The results suggest that rutin may be useful in the treatment of desflurane-associated lung injury.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021Protective 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Effect of taxifolin on cisplatin-associated oxidative optic nerve damage in rats
Ahiskali, Ibrahim; Ferah Okkay, Irmak; Mammadov, Renad; Okkay, Ufuk; Keskin Cimen, Ferda; Kurt, Nezahat; Suleyman, Halis
Aim: To investigate the effect of taxifolin on cisplatin-induced oxidative and proinflammatory optic nerve damage in rats. Methods: A total of 18 albino Wistar male rats were assigned into 3 groups, as follows; Group 1: Control group, Group 2: Only cisplatin administered group for 14 days (Cisplatin group), and Group 3: Taxifolin + cisplatin administered group for 14 days (CIS + TAX group). Serum malondialdehyde (MDA), total Glutathione (tGSH), Nuclear Factor-Kappa B (NF-ƘB), Total Oxidative Status (TOS) and Total Antioxidant Status (TAS) levels were collected from the left eyes of rats. Rats’ right eyes were enucleated for histopathological evaluations of optic nerves. Results: NF-ƘB, MDA and TOS levels were statistically significantly higher (p < 0.001) in cisplatin group when compared to other 2 groups, the tGSH and TAS levels of which were statistically significantly lower (p < 0.001). Regarding these parameters, in cisplatin group NF-ƘB, MDA and TOS levels were statistically significantly increased with cisplatin administration and giving taxifolin concomitantly with cisplatin prevented this elevation. On the other hand, tGSH and TAS levels were statistically significantly decreased with cisplatin administration and routine simultaneous application of taxifolin with cisplatin prevented this decrease. In histopathological findings, haemorrhage was observed in the perineum of the injured optic nerves in the cisplatin treated group. And also edoema and degeneration in nerve fascicles in damaged optic nerves were seen in the cisplatin group. In the taxifolin treated group histopathological examinations were close to normal appearance, except mild edoema in nerve fascicles. Conclusion: Cisplatin causes oxidative stress on the rat optic nerves, and these changes lead to significant histopathological damage. Taxifolin, which we used to prevent oxidative damage to the optic nerves caused by cisplatin, has been emphasized as a powerful antioxidant agent in many previous scientific investigations. Concomitant administration of taxifolin may prevent these adverse effects of cisplatin, as well as histopathological damage. Further studies are needed to fully determine the effects of cisplatin and taxifolin on the eye.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021The effect of adenosine triphosphate on bevacizumab-induced ovarian damage and reproductive dysfunction in rats
Ince, Sefa; Ozer, Mehmet; Kadioğlu, Berrin Goktug; Kuzucu, Mehmet; Yilmaz, Sevil Karahan; Özkaraca, Mustafa; Gezer, Arzu; Suleyman, Halis
We investigated the effect of ATP’s protection against possible bevacizumab-induced ovarian damage and reproductive dysfunction in female albino Wistar rats. A total of 42 rats, 36 females, and 6 males were used in the experiment. Normal saline (0.9% NaCl) was injected as a solvent to the Bevacizumab (BVZ; n = 12) and Control (n = 6) groups. 25 mg/kg ATP was injected intraperitoneally (i.p.) to the ATP + bevacizumab (ABZ; n = 12) group. One hour after ATP and solvent administration, 10 mg/kg bevacizumab was i.p. injected to the ABZ and BVZ groups. Bevacizumab was administered once a day every two weeks; ATP was administered one a day for 30 days. At the end of this period, six rats from each group were sacrificed with high dose of anesthesia (thiopental sodium 50 mg/kg) and biochemical and histopathological examinations were performed in ovarian tissues. Mature male rats were kept in the laboratory for two months to breed the remaining female animals. The values showed that the oxidant parameters increased in the ovarian tissue of the BVZ group compared to the healthy controls and the ABZ group, while antioxidant parameters decreased. The number of breeding animals was significantly decreased in the BVZ group compared to the Control and the ABZ groups. This result suggests that ATP may be effective in preventing oxidative damage to the ovaries and infertility induced by bevacizumab.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021The effect of taxifolin on oxidative ovarian damage and reproductive dysfunctions induced by antipsychotic drugs in female rats
Ince, Sefa; Ozer, Mehmet; Kadioglu, Berrin Goktug; Kuzucu, Mehmet; Ozkaraca, Mustafa; Gezer, Arzu; Suleyman, Halis; Cetin, Nihal
Aim: Typical antipsychotics (TAPs) are commonly used to treat schizophrenia and bipolar disorder. However, extrapyramidal disorders, hyperprolactinemia, and reproductive dysfunctions have been observed in women during the use of TAPs. For this reason, less toxic and prolactin-sparing atypical antipsychotic (AAP) drugs such as clozapine (CLN) have been developed. The aim of this study is to investigate the effect of taxifolin on possible ovarian and reproductive toxicity associated with CLN and haloperidol (HPL) in female Wistar albino rats. Methods: The rats were grouped as healthy control group (HCG), CLN, HPL, taxifolin + clozapine (TCL), and taxifolin + haloperidol (THL). Drugs were administered to the groups for 28 days. At the end of that time, ovarian tissues of six rats from each group were taken for histopathological and biochemical analyses. Remaining six rats in groups were examined for evaluation of reproductive dysfunctions. Results: Severe degeneration and vacuolization were observed in the primary, secondary, and primordial follicles of the ovarian tissues of CLN- and HPL-treated groups, of which malondialdehyde (MDA) level was high and total glutathione (tGSH) level was low. In the taxifolin-treated groups, taxifolin significantly prevented the increase of MDA level and decrease of tGSH level, and the severity of histopathological damage was found to be lower. In addition, it was found that taxifolin significantly prevented infertility and delay in pregnancy associated with CLN and HPL. Conclusions: The results of this experiment suggest that taxifolin can be beneficial in treating oxidative ovarian damage, infertility, and reproductive dysfunctions induced by CLN and HPL.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Effect 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.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021The effect of Hippophae rhamnoides L. Extract on acrylamide-induced brain injury in rats
Turan, Mehmet Ibrahim; Aktaş, Mehmet; Gundogdu, Betul; Yilmaz, Sevil Karahan; Suleyman, Halis
Purpose: Reactive oxygen species (ROS), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1β and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically. Methods: To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically. Results: It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1β and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue. Conclusion: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021Protective effects of taxifolin on pazopanib-induced liver toxicity: An experimental rat model
Akagunduz, Baran; Ozer, Muhammet; Ozcıcek, Fatih; Kara, Ali Veysel; Lacın, Sahin; Özkaraca, Mustafa; Çoban, Abdulkadir; Suleyman, Bahadır; Mammadov, Renad; Suleyman, Halis
Pazopanib is a tyrosine kinase inhibitor that is generally used for the treatment of metastatic renal cell cancer and advanced soft tissue sarcoma. It can cause various degrees of hepatotoxicity. Our study aimed to investigate the effect of taxifolin on pazopanib-induced liver toxicity. A total of 18 rats were divided into three groups: the pazopanib (PP), pazopanib plus taxifolin (TPP), and control (C) group. Taxifolin was administered to the TPP (n=6) group with a dose of 50 mg/kg. Distilled water was orally admnistered to the C (n=6) and PP (n=6) groups as a solvent. Subsequently, pazopanib 200 mg/kg was administered to the TPP and PP groups via the stomach. This procedure was repeated once a day for four weeks. Then, all rats were sacrificed, and their livers were removed. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS), and total antioxidant status (TAS) levels were evaluated. MDA and TOS levels were higher in the PP group compared with the levels of the other parameters (P<0.001). tGSH and TAS levels were lower in the PP group than in the TPP and C groups (P<0.001), and the aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) levels were higher. Furthermore, liver tissue damage, including hemorrhage, hydropic degeneration, and necrosis was observed in the PP group. Administration of taxifolin before pazopanib significantly improved degenerative changes. Our study demonstrated that the administration of taxifolin is significantly effective in preventing pazopanib-induced hepatotoxicity in rats.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021The 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.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021Protective 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.
RDL Kalıcı Kaydıİncele - ArticleAçık Erişim2021Effect 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021The 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.
RDL Kalıcı Kaydıİncele - ArticleYalnız künye2021Effect 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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