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    Arbutin abrogates cisplatin-induced hepatotoxicity via upregulating Nrf2/HO-1 and suppressing genotoxicity, NF-?B/iNOS/TNF-? and caspase-3/Bax/Bcl2 signaling pathways in rats
    (Oxford Univ Press, 2024) Okkay, Irmak Ferah; Famurewa, Ademola; Bayram, Cemil; Okkay, Ufuk; Mendil, Ali Sefa; Sezen, Selma; Ayaz, Teslime
    Background: Cisplatin is a potent anticancer agent widely employed in chemotherapy. However, cisplatin leads to toxicity on non-targeted healthy organs, including the liver. We investigated the hepatoprotective mechanism of arbutin (ARB), a glycosylated hydroquinone, against cisplatin-induced hepatotoxicity. Methods: Rats were orally administered with ARB (ARB1 = 50 mg/kg; ARB2 = 100 mg/kg) for 14 consecutive days against hepatotoxicity induced by a single dose of cisplatin (10 mg/kg) on day 15. Three days after the intraperitoneal cisplatin injection, serum and liver tissue were collected for subsequent analyses. Results: Cisplatin triggered marked increases in serum AST, ALT, and ALP activities, hepatic malondialdehyde (MDA) and reactive oxygen species (ROS) coupled with a considerable diminution in hepatic activities of superoxide dismutase (SOD), catalase (CAT) and the concentration of reduced glutathione (GSH). The gene expressions of interleukin-1 beta (IL-1 beta), tumor necrosis factor (TNF-alpha), and IL-6 were notably increased. The pre-administration of ARB1 and ARB2 reduced AST, ALT and ALP in serum and restored SOD, CAT, GSH, ROS, MDA and cytokine levels which was also evidenced by alleviated hepatic lesions. Further, cisplatin-induced prominent alterations in the gene expressions of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), iNOS, NF-kappa B, Bax, Bcl-2, caspase-3 and 8-OHdG in the liver. Interestingly, ARB protected the liver and mitigated the cisplatin-induced alterations in serum AST, ALT, ALP, and reduced hepatic redox markers, 8-OdG, inflammatory markers and gene expressions. Conclusion: The findings demonstrate that ARB is a potential protective adjuvant against cisplatin-induced hepatotoxicity via inhibition of hepatic oxidative stress, inflammation, and apoptosis.
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    Assessment of antimicrobial activity and In Vitro wound healing potential of ZnO nanoparticles synthesized with Capparis spinosa extract
    (Ekim 2023) Sezen, Selma; Ertuğrul, Muhammed Sait; Balpınar, Özge; Bayram, Cemil; Özkaraca, Mustafa; Okkay, Irmak Ferah; Hacımüftüoğlu, Ahmet; Güllüce, Medine
    Agents that will accelerate wound healing maintain their clinical importance in all aspects. The aim of this study is to deter mine the antimicrobial activity of zinc oxide nanoparticles (ZnO NPs) ZnO nanoparticles obtained by green synthesis from Capparis spinosa L. extract and their efect on in vitro wound healing. ZnO NPs were synthesized and characterized using Capparis spinosa L. extract. ZnO NPs were tested against nine ATCC-coded pathogen strains to determine antimicrobial activity. The efects of diferent doses (0.0390625–20 µg/mL) of NPs on cell viability were determined by MTT assay. The efect of ZnO NPs doses (0.0390625 µg/mL, 0.078125 µg/mL, 0.15625 µg/mL, 0.3125 µg/mL, 0.625 µg/mL, 1.25 µg/mL) that increase proliferation and migration on wound healing was investigated in an in vitro wound experiment. Cell culture medium obtained from the in vitro wound assay was used for biochemical analysis, and plate alcohol-fxed cells were used for immunohistochemical staining. It was determined that NPs formed an inhibition zone against the tested Gram-positive bacteria. The ZnO NPs doses determined in the MTT test provided faster wound closure in in-vitro conditions compared to the DMSO group. Biochemical analyses showed that infammation and oxidative status decreased, while antioxidant levels increased in ZnO NPs groups. Immunohistochemical analyses showed increased expression levels of Bek/FGFR2, IGF, and TGF-β associated with wound healing. The fndings reveal the antimicrobial efect of ZnO nanoparticles obtained using Capparis spinosa L. extract in vitro and their potential applications in wound healing.
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    Assessment of antimicrobial activity and In Vitro wound healing potential of ZnO nanoparticles synthesized with Capparis spinosa extract
    (Springer Heidelberg, 2023) Sezen, Selma; Ertugrul, Muhammed Sait; Balpinar, Ozge; Bayram, Cemil; Ozkaraca, Mustafa; Okkay, Irmak Ferah; Hacimuftuoglu, Ahmet
    Agents that will accelerate wound healing maintain their clinical importance in all aspects. The aim of this study is to determine the antimicrobial activity of zinc oxide nanoparticles (ZnO NPs) ZnO nanoparticles obtained by green synthesis from Capparis spinosa L. extract and their effect on in vitro wound healing. ZnO NPs were synthesized and characterized using Capparis spinosa L. extract. ZnO NPs were tested against nine ATCC-coded pathogen strains to determine antimicrobial activity. The effects of different doses (0.0390625-20 mu g/mL) of NPs on cell viability were determined by MTT assay. The effect of ZnO NPs doses (0.0390625 mu g/mL, 0.078125 mu g/mL, 0.15625 mu g/mL, 0.3125 mu g/mL, 0.625 mu g/mL, 1.25 mu g/mL) that increase proliferation and migration on wound healing was investigated in an in vitro wound experiment. Cell culture medium obtained from the in vitro wound assay was used for biochemical analysis, and plate alcohol-fixed cells were used for immunohistochemical staining. It was determined that NPs formed an inhibition zone against the tested Gram-positive bacteria. The ZnO NPs doses determined in the MTT test provided faster wound closure in in-vitro conditions compared to the DMSO group. Biochemical analyses showed that inflammation and oxidative status decreased, while antioxidant levels increased in ZnO NPs groups. Immunohistochemical analyses showed increased expression levels of Bek/FGFR2, IGF, and TGF-beta associated with wound healing. The findings reveal the antimicrobial effect of ZnO nanoparticles obtained using Capparis spinosa L. extract in vitro and their potential applications in wound healing.
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    Effects of Rhodiola rosea on indomethacin-induced gastric injury
    (2021) Okkay, Irmak Ferah; Okkay, Ufuk; Karataş, Özhan
    Objective: The objective of the present study was to evaluate the effects of Rhodiola rosea in the indomethacin-induced ulcer model in rats and to clarify the underlying mechanisms of action. Methods: Rats in treatment groups were treated with Rhodiola rosea (RR) 14 days. Peptic ulcer was induced by indomethacin (IND) injection (100 mg/kg, p.o.). The groups (n = 6) were designed as; Group I (control); Group II (IND): After 24h of food starvation, rats were given only 100 mg/kg IND by oral gavage to induce gastric mucosal injury. Group III (ESO): Rats were pretreated with 20 mg/kg of ESO for 14 consecutive days by oral gavage. Group IV (RR): Rats were pretreated with 500 mg/kg RR for 14 consecutive days with oral gavage. Results: Rhodiola rosea effectively alleviated indomethacin-induced ulcer via reduction in oxidative stress (decreased MDA and increased SOD, and GSH). Moreover, Rhodiola rosea alleviated indomethacin-induced damage by regulating expressions of COX enzymes, prostaglandin E2, proliferating cell nuclear antigen (PCNA), cell proliferation, apoptosis and regulated the NF-?B signaling pathway. Rhodiola rosea also attenuated inflammatory injury by suppressing TNF-????, IL-1?, and NF-?B. The caspase-3 expression was also down-regulated in stomach tissues. Conclusions: In conclusion, Rhodiola rosea protected the gastric mucosa from harmful effects of indomethacin and as a natural medicinal herb, Rhodiola rosea might be a potential therapeutic agent for preventing and treating indomethacin-induced gastric damage.
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    Hepatoprotective and neuroprotective effect of taxifolin on hepatic encephalopathy in rats
    (Springer/Plenum Publishers, 2022) Okkay, Ufuk; Okkay, Irmak Ferah; Cicek, Betul; Aydin, Ismail Cagri; Ozkaraca, Mustafa
    This study was planned to assess the potential protective effects of taxifolin against thioacetamide-induced hepatic encephalopathy and subsequently to portray its behavioural results. The experimental model was induced with three doses of (200 mg/kg i.p.) thioacetamide and taxifolin (50 and 100 mg/kg, p.o.) was administered for fourteen days. Taxifolin effectively attenuated hepatic encephalopathy through decrease in AST, ALT, ALP and LDH concentrations and improvement of hyperammonemia, and increase in antioxidant capacity by decreasing MDA, ROS, and increasing CAT and GSH. In addition, the expressions of NF-kappa B, TNF-alpha, IL-1 beta, caspase-3 and Bax was down-regulated while IL-10 and Bcl-2 expressions were up-regulated with taxifolin treatment. The recovery was confirmed by downregulation of iNOS and 8-OHdG expressions in our immunohistochemical analysis. Taxifolin treatment reduced the disrupting role of thioacetamide as seen by corrected hyperammonemia as well as preservation of astrocyte and hepatocyte structure. Elevated plus maze and locomotor activity tests also proved that taxifolin might repeal the neurobehavioral disabilities. In conclusion, taxifolin has shown hepatoprotective and neuroprotective roles with antioxidant and anti-inflammatory effects, as well as suppressing the excessive release of ammonia, and it eventually reversed neurobehavioral impairments.
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    Syringic acid guards against indomethacin-induced gastric ulcer by alleviating inflammation, oxidative stress and apoptosis
    (Taylor & Francis Ltd, 2024) Okkay, Irmak Ferah; Okkay, Ufuk; Cicek, Betul; Karatas, Ozhan; Yilmaz, Aysegul; Yesilyurt, Fatma; Hacimuftuoglu, Ahmet
    The purpose of this study was to evaluate the effects of syringic acid, an anti-oxidant, on indomethacin induced gastric ulcers in rats. Experimental groups were control, ulcer, ulcer treated with 20 mg/kg esomeprazole (a proton pump inhibitor that reduces acid secretion), and ulcer treated with 100 mg/kg syringic acid. Rats were pretreated with esomeprazole or syringic acid two weeks before ulcer induction. Our histopathological observations showed that either syringic acid or esomeprazole attenuated the severity of gastric mucosal damage. Moreover, syringic acid and esomeprazole pretreatments alleviated indomethacin-induced damage by regulating oxidative stress, inflammatory response, the level of transforming growth factor-beta (TGF-beta), expressions of COX and prostaglandin E2, cell proliferation, apoptosis and regulation of the NF-kappa B signaling pathway. We conclude that either esomeprazole or syringic acid administration protected the gastric mucosa from harmful effects of indomethacin. Syringic acid might, therefore be a potential therapeutic agent for preventing and treating indomethacin-induced gastric damage.