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    Evaluation of Retinol Palmitate Treatment of Photokeratitis in Rat Eyes Exposed to Ultraviolet B Radiation
    (2019) Filizay, Mehmet Caner; Gökçınar, Nesrin Büyüktortop; Şahintürk, Varol; Öner, Kevser Setenay; Kaçar, Sedat; Onaran, Zafer; Yumuşak, Mehmet Erhan
    Objectives: Acute exposure to ultraviolet B radiation can cause photokeratitis. Retinol palmitate (RP) is known to have antioxidant properties and improve corneal healing. The aim of this study was to evaluate the effect of topical RP against phototoxic keratitis in rats.Methods: A total of 14 male Wistar Albino rats were exposed to 1 J/cm2 dose of 311 nm ultraviolet B radiation. The subjects were then divided into 4 study groups using the right and left eye: The RP-5 group (n7) received topical 250 IU/g RP ointment and the Sham-5 group (n7) received only the vehicle base component of the ointment 5 minutes after the exposure. The RP-120 group (n7) received topical RP and the Sham-120 group (n7) received the vehicle alone 120 min-utes after the exposure. The eyes were enucleated 24 hours after the exposure and stained with hematoxylin and eosin for histopathological examination and a terminal deoxynucleotidyl transferase dUTP nick end labeling assay to test for apoptosis.Results: There was no statistically significant difference between the mean corneal epithelial thickness of the RP-5 group and the Sham-5 group (p0.369). Furthermore, there was no significant difference between the RP-120 and the Sham-120 groups (p0.765). The timing of the administration of RP resulted in no significant difference in the mean corneal epithelial thickness (p0.608). Apoptotic cell count scores were not significantly different between corneas that received RP and those who received only the vehicle (p0.530, p0.107).Conclusion: Topical administration of a single dose of RP was not superior to the use of the vehicle base alone in a photokeratitis model produced using 1 J/cm2 of narrowband ultraviolet radiation in rats.
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    Protective Effects of Boron on Cyclophosphamide-Induced Bladder Damage and Oxidative Stress in Rats
    (HUMANA PRESS INC, 2020) Ayhancı, Adnan; Tanriverdi, Döndü Tuğçe; Şahintürk, Varol; Cengiz, Mustafa; Appak-Baskoy, Sıla; Şahin, İlknur Kulcanay
    This study aims to investigate protective effects of boron against cyclophosphamide-induced bladder toxicity that produces oxidative stress and leads to apoptosis of the cells. In total, 24 rats were divided into 4 equal groups. The control group received saline. The 2nd experimental group received 200 mg kg of cyclophosphamide i.p. on the 4th day while the 3rd group was given only boron (200 mg kg, i.p.) for 6 days. In the 4th group, boron was given for 6 days and cyclophosphamide (200 mg kg, i.p.) was administrated on the 4th day. Twenty-four hours after the last boron or cyclophosphamide administration, rats were sacrificed under anesthesia. Bladder tissues of rats were taken for histological and immunohistochemical (apoptotic markers such as caspase-3, bcl-2, and bax) and blood was taken for the biochemical (serum total thiol, serum natural thiol, serum thiol-disulfide) analysis. Transient epithelial thinning, edema, marked inflammatory reaction, and bleeding were observed in bladders of the group that received cyclophosphamide. Also, the activity of bax and caspase-3-positive cells increased while the number of bcl-2-positive cells decreased. In the same group, serum natural thiol and total thiol levels decreased while serum disulfide levels increased, which indicates oxidative stress. On the other hand, in the boron+cyclophosphamide group pretreatment with boron protected, the bladder tissue and the number of bcl-2-positive cells increased, and bax and caspase-3-positive cells decreased, showing antiapoptotic effects of boron against cyclophosphamide-induced toxicity. In parallel with the findings of this group, native thiol and total thiol levels increased and serum disulfide levels decreased pointing out to a decreased oxidative stress. Our results indicate that boron pretreatment significantly protects rat bladder against cyclophosphamide-induced bladder damage due to its antiapoptotic and antioxidant properties.
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    Öğe
    The protective effects of selenium and boron on cyclophosphamide-induced hepatic oxidative stress, inflammation, and apoptosis in rats
    (Elsevier Ltd, 2024) Cengiz, Mustafa; Gür, Bahri; Gür, Fatma; Şahintürk, Varol; Bayrakdar, Alpaslan; Şahin, Ilknur Kulcanay; Başkoy, Sıla Appak
    Cyclophosphamide (CP) is an alkylating anticancer drug with broad clinical application that is highly effective in the treatment of cancer and non-malignant diseases. However, the main limiting effect of CP is multi-organ toxicity due to damage to normal tissues. The aim of this study is to compare the hepatoprotective potential of selenium (Se) and boron (B) in CP-induced liver injury in experimental rats. The rats were randomly divided into six equal groups: Control (saline), 200 mg/kg CP (administered once on the fourth day of the experiment), 1.5 mg/kg Se (administered once/time daily for 6 days), 20 mg/kg B (administered once/time daily for 6 days), Se + CP and B + CP administered intraperitoneally (i.p.). Administration of CP leads to an increase in the levels of apoptotic markers (Bax, caspase-3), the apoptotic signaling pathway (Nrf2), oxidative stress indicators (TOS, OSI), lipid peroxidation markers (MPO, MDA), inflammation levels (NF-kB, TNF-?, IL-1?, IL -6), liver function markers (ALT, AST, ALP), while apoptosis markers (Bcl-2), apoptosis pathway (Keap-1), oxidative stress indicator (TAS), inflammation (IL -10) and intracellular antioxidant defense system (SOD, CAT, GPx and GSH) decreased. In addition, degeneration of hepatocytes and congestion in the central veins were observed. In contrast, in the groups administered Se and B with CP, the changes that occurred were reversed. However, it was found that Se protects the liver slightly better against CP damage than B. The protective effect of Se and B against the toxic effects of CP on the antioxidant markers SOD, CAT and GPx1 was also investigated in silico. The in silico results were consistent with the in vivo results for SOD and CAT, but not for GPx1. © 2024