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    Beneficial effects of ?-glucan against cisplatin side effects on the nervous system in rats
    (Acta Cirurgica Brasileira, 2016) Kaya, Kursat; Ciftci, Osman; Cetin, Asli; Tecellioglu, Mehmet; Basak, Nese
    PURPOSE: To investigate the protective effect of Bg on cisplatin (CP)-induced neurotoxicity in rats. METHODS: Twenty eight rats were randomly distributed into four groups. The first group was kept as a control. In the second group, CP was given at the single dose of 7 mg/kg intraperitoneally. In the third group, beta g was orally administered at the dose of 50 mg/kg/day for 14 days. In the fourth group, CP and beta g were given together at the same doses. RESULTS: CP treatment caused significant oxidative damage via induction of lipid peroxidation and reductions antioxidant defense system potency in the brain tissue. In addition, histopathological damage increased with CP treatment. On the other hand, beta g treatment largely prevented oxidative and histopathological negative effects of CP. CONCLUSIONS: Cisplatin has severe neurotoxic effects in rats and ag supplementation has significant beneficial effects against CP toxicity depending on its antioxidant properties. Thus, it appears that Ag might be useful against CP toxicity in patients with cancer in terms of nervous system.
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    Beta-glucan attenuates cerebral ischemia/reperfusion-induced neuronal injury in a C57BL/J6 mouse model
    (Univ Sao Paulo, Conjunto Quimicas, 2019) Kaya, Kursat; Ciftci, Osman; Oztanir, Mustafa Namik; Taslidere, Elif; Turkmen, Nese Basak
    Beta-glucans (beta g), that have many useful effects on human health, are natural polysaccharides. Our aim in this study was to determine useful effect of beta g against oxidative and neuronal damage caused by global cerebral ischemia/reperfusion (IR) in stroke imitated mice via surgical operation. A total of 40 mice divided into four equal groups randomly. The group 1 (sham operated) was kept as control. Bilateral carotid arteries of subjects in group 2 (I/R) and group 4 (I/R + beta g) were clipped for 15 min, and the mice in group 4 (I/R + beta g) were treated with beta g (50 mg/kg/day), while the mice in group 2 (I/R) were treated with only vehicle for 10 days. The mice of group 3 (beta g) were treated with beta g for 10 days without carotid occlusion. Global cerebral I/R significantly increased oxidative stress and decreased members of anti-oxidant defense system. In addition, I/R caused histopathological damage in the brain tissue. However, beta g treatment ameliorated both oxidative and histopathological effects of I/R. Our present study showed that beta g treatment significantly ameliorated oxidative and histological damage in the brain tissue caused by cerebral I/R. Therefore, beta g treatment can be used as supportive care for ischemic stroke patients.
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    Favourable effect of ?-glucan treatment against cisplatin-induced reproductive system damage in male rats
    (Wiley, 2019) Kaya, Kursat; Ciftci, Osman; Aydin, Muhterem; Cetin, Asli; Basak, Nese
    The aim of this study was to investigate the potential beneficial effects of beta-glucan treatment against oxidative, histological and spermatological damage caused by cisplatin on the male reproductive system. Twenty-eight Sprague Dawley male rats were used in the study. The rats were randomly divided into four equal-sized groups: a control group, cisplatin group (7 mg/kg in a single-dose cisplatin administered intraperitoneally), beta-glucan group (beta-glucan given at a dose of 50 mg kg(-1) d(-1) for 14 day) and a cisplatin plus beta-glucan group (cisplatin and beta-glucan administered together at the same dose). Cisplatin administration induced an increase in the level of thiobarbituric acid-reactive substances, a lipid peroxidation indicator. It induced a decrease in enzymatic (superoxide dismutase, catalase and glutathione peroxidase) activities and nonenzymatic (reduced glutathione) antioxidant levels. In addition, cisplatin caused both histological and spermatological damage, as shown by a decrease in sperm motility and epididymal sperm concentrations and an increase in abnormal sperm rates. The beta-glucan treatment improved cisplatin-induced oxidative, histological and spermatological damage. This study revealed that beta-glucan treatment provided prevention against male reproductive system damage caused by cisplatin. These preventative effects were likely due to its antioxidant properties.
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    Fish oil protects the peripheral and central nervous systems against cisplatin-induced neurotoxicity
    (Maney Publishing, 2014) Kamisli, Suat; Ciftci, Osman; Cetin, Asli; Kaya, Kursat; Kamisli, Ozden; Celik, Hamit
    Objective: The protective effects of fish oil (FO) on cisplatin (CP)-induced central and peripheral neurotoxicity were investigated in rats. Methods: Rats (n = 28) were divided equally into four groups, the first group was kept as a control. In the second and third groups, CP and FO were given at doses of 7 mg/kg and 1 softgel/rat/day, respectively. In the fourth group, CP and FO were given together at the same doses. Results: Although CP caused significant oxidative damage, via induction of lipid peroxidation and reduction in the antioxidant defense system potency, FO treatment largely reversed these effects. CP also resulted in histopathological damage, such as apoptosis, and electromyographical changes in the sciatic nerve. FO treatment partially prevented the histopathological and electromyographical effects of CP. Discussion: CP has severe central and peripheral neurotoxic effects in rats and these effects were largely prevented by FO treatment. Thus, it appears that co-administration of FO with CP may be a useful approach to attenuate the negative effects of CP on the nervous system.
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    ?-Glucan ameliorates cisplatin-induced oxidative and histological damage in kidney and liver of rats
    (Taylor & Francis Ltd, 2024) Kaya, Kursat; Ciftci, O.; Turkmen, N. Basak; Taslidere, A.; Gul, C. C.
    We investigated the effects of beta-glucan (beta g) on kidney and liver damage caused by cisplatin (CP), an antineoplastic agent widely used to treat many types of cancer, in a rat model. The side effects of CP in many tissues and organs limit its usage. beta g is a natural polysaccharide that is an effective free radical scavenger. A total of 28 rats were randomly divided into four groups. Group 1 was a non-intervention control, only feed and water were given. Group 2 was administered 7 mg/kg CP in a single dose. Group 3 was administered 50 mg/kg beta g orally for 14 days. Group 4 was administered beta g for 14 days, following a single dose of CP. At the end of the experiment, kidney and liver tissues were evaluated biochemically and histopathologically. Increased thiobarbituric acid-reactive substances (TBARS) levels, as well as decreased catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) levels, as well as histological damage, were noted in both the kidney and liver tissues of the CP group. However, beta g treatment prevented the oxidative and histopathological effects of CP. The study demonstrates the protective efficacy of beta g against CP-induced kidney and liver damage through the effect of its antioxidant properties.
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    Hesperidin protects brain and sciatic nerve tissues against cisplatin-induced oxidative, histological and electromyographical side effects in rats
    (Sage Publications Inc, 2015) Kamisli, Suat; Ciftci, Osman; Kaya, Kursat; Cetin, Asli; Kamisli, Ozden; Ozcan, Cemal
    In the present study, the beneficial effect of hesperidin (HP), a citrus flavonoid, on cisplatin (CP)-induced neurotoxicity was investigated. A total of 28 rats were equally divided into four groups; the first group was kept as control. In the second and third groups, CP and HP were given at the doses of 7 and 50 mg/kg/day, respectively. In the fourth group, CP and HP were given together at the same doses. The results indicated that although CP caused significant induction of lipid peroxidations and reduction in the antioxidant defense system potency in the brain and sciatic nerve, HP prevented these effects of CP. Besides, CP led to histopathological damage, mainly apoptosis, as well as electromyographical (EMG) changes in sciatic nerve. On the other hand, HP treatment reversed histopathological and EMG effects of CP. In conclusion, CP had severe dose-limiting neurotoxic effects and these effects of CP can be prevented by HP treatment. Thus, it appears that coadministration of HP with CP may be a useful approach to attenuate the negative effects of CP on the nervous system.