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    Nephroprotective effect of aloe vera extract with regulation of oxidative stress, apoptosis and aquaporin 3 expression levels in streptozotocin induced diabetic rats
    (Ankara Üniversitesi Eczacılık Fakültesi, 2023) Şeker, Uğur; Güzel, Barış Can; Akçora, Dila Şener; Baygeldi, Saime Betül; Yüksel, Meral; Demirel, Özlem Unay; Söker, Sevda
    Objective: In this study we examined the protective activity of Aloe vera with considering anti-oxidant, anti-apoptotic properties, and the status of Aquaporin 3 (AQP3) channel protein. Material and Method: Twenty-one adult female rats were divided into three groups (n=7); Control, Diabetes, Treatment. Control group did not expose to any application. Animals in Diabetes and Treatment were exposed to experimental diabetes with administration of streptozotocin. Rats in Treatment received 300 mg/kg Aloe vera extract daily for 14 days. Rats were sacrificed and kidney samples were used for analyses. Result and Discussion: Analyses indicated that lowest malondialdehyde (MDA) and luminol levels in control group were increased significantly (P<0.05) in diabetic animals. Severe pathological changes observed in Diabetes group while microscopic examinations. Bax, Caspase-3 and apoptotic index (AI) were elevated significantly (P<0.05) in this group compared to Control. Oxidative stress, apoptotic protein expression levels and TUNEL Assay positive cell ratio were down-regulated in Treatment group. When AQP3 levels were measured, immunopositivity reduced significantly (P<0.05) in cortical kidney of Diabetes group which is normalized significantly in Treatment group.This study reporting anti-diabetic potency of Aloe vera extract has capability to avoid streptozotocin induced diabetic renal injury via regulating anti-apoptotic and anti-oxidant cellular signaling. Furthermore, Aloe vera consumption in diabetes might regulate AQP3 levels. Although we observed promising results, more studies are required to explore anti-diabetic, anti-hyperglycemic and nephroprotective activity of Aloe vera.
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    Targeting soluble guanylate cyclase with Riociguat has potency to alleviate testicular ischaemia reperfusion injury via regulating various cellular pathways
    (John Wiley and Sons Inc, 2022) Şeker, Uğur; Kavak, Deniz Evrim; Güzel, Barış Can; Baygeldi, Saime Betül; Yüksel, Meral; Kandemir, Sevgi İrtegün; Şener, Dila; Demirel, Özlem Unay
    Testicular ischaemia reperfusion (I/R) injury results with serious dysfunctions in testis. This study aims to explore effects of soluble guanylate cyclase (sGC) stimulator Riociguat on experimental testicular I/R injury in rats. Twenty-one male rats were divided into three groups (Control, IR and IRR). The control group was not exposed to any application. Bilateral testis from IR and IRR animals were rotated 720° in opposite directions for 3 h to induce experimental testicular ischaemia. Animals in IR and IRR groups were subjected to 3 h of reperfusion. Isotonic and Riociguat were administered to the animals 30 min prior reperfusion by oral gavage. At the end of experiment, animals were sacrificed and tissue samples were used for analyses. Riociguat treatment significantly decreased tissue malondialdehyde and Luminol levels compared to the IR group (p < 0.05). The pathological changes, pro-apoptotic proteins (Bax, Caspase 3, and Caspase 9) and apoptotic index in the IR group were down regulated in Riociguat treated animals (p < 0.05). Riociguat treatment was also significantly increased anti-apoptotic Bcl-2 expression, but alleviated tissue injury via modulating pro-inflammatory cytokine IL-1β levels and significantly (p < 0.05) down-regulating NF-κB activity. Moreover, mTOR and ERK phosphorylation increased in IR group (p < 0.05), but Riociguat treatment reduced protein phosphorylation. Our experiment indicated that targeting sGC might support surgical interventions in testicular I/R injury by modulating oxidative stress, inflammation, and apoptotic protein expression levels, but more detailed studies are required to explore the protective activity of Riociguat and underlying mechanisms in testicular I/R injury.