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ÖZDEMİR KUMRAL, ZARİFE NİGAR

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ÖZDEMİR KUMRAL

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ZARİFE NİGAR

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2017 - 20182
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Author: ERCAN, FERİHA × Subject: DAMAGE ×

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    Protective effect of ferulic acid on cisplatin induced nephrotoxicity in rats
    (ELSEVIER, 2017) OKUYAN, BETÜL; Bami, Erliasa; Ozakpinar, Ozlem Bingol; Ozdemir-Kumral, Zarife Nigar; Koroglu, Kutay; Ercan, Feriha; Cirakli, Zeynep; Sekerler, Turgut; Izzettin, Fikret Vehbi; Sancar, Mesut; Okuyan, Betul
    This study aims to determine the potential protective effects of ferulic acid against cisplatin-induced nephrotoxicity and to compare its effect with curcumin, a well-known protective agent against cisplatin- induced toxicity in rats. Administration of cisplatin resulted in high BUN (Blood Urea Nitrogen), creatinine, MDA (Malondialdehyde), MPO (Myeloperoxidase), TOS (Total Oxidative Status), PtNT (Protein Nitrotyrosine) levels (p < 0.05). Histological observations showed abnormal morphology of kidney; in addition with appearance of TUNEL positive cells indicating apoptosis in cisplatin administered group. HO-1 (Heme Oxygenase-1) levels measured by RT-PCR (Real Time Polymerase Chain Reaction), and TAS (Total Antioxidative Status) revealed antioxidant depletion due to cisplatin toxicity in animals (p < 0.05). All parameters showed improvement in groups treated with ferulic acid (p < 0.05). Ferulic acid treatment was found significant in preventing oxidative stress, increasing antioxidative status and regaining histological parameters to normal, indicating nephroprotective and antioxidant effects of this phenolic compound.
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    Nesfatin-1 Ameliorates Sepsis-Induced Remote Organ Injury: The Role of Oxidant-Antioxidant Status and Neutrophils
    (MARMARA UNIV, INST HEALTH SCIENCES, 2018) YEGEN, BERRAK; Ozdemir-Kumral, Zarife Nigar; Cumhur, Ahmet; Oluk, Ali Ihsan; Hoscan, Aykut; Onem, Idris; Contuk, Gazi; Ercan, Feriha; Yegen, Berrak C.
    Purpose: Protective effects of nesfatin-1 was studied in sepsis-induced injury of remote organs. Methods: Male rats were randomly divided as control and sepsis (cecal ligation-perforation) groups, treated with either saline or nesfatin-1 (10 mu g/kg). At 16 h following surgery, samples of brain, kidney, liver and lung tissues were removed and myeloperoxidase (MPO) activity, glutathione (GSH), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured in these tissues. Results: In saline-treated septic rats, elevated MDA and MPO activities were accompanied with depleted CAT, SOD and GSH levels in the brain, kidney, liver and lung tissues, implicating extensive oxidative damage in all remote organs. Nesfatin-1 reduced MDA levels (brain, lung) and MPO activities (brain, kidney), and preserved antioxidant GSH (brain, lung), CAT (brain) and SOD (kidney) levels. Severe hepatocyte degeneration, neuronal damage, glomerulotubular degeneration and alveolar disturbance in saline-treated septic rats were replaced with regular tissue morphologies in nesfatin-1-treated rats. Conclusion: Nesfatin-1 alleviates oxidative damage by enhancing endogenous antioxidant systems and inhibiting recruitment of neutrophils, suggesting that nesfatin-1 may be have a potential therapeutic impact on the treatment of septic shock to reduce subsequent remote organ failure.