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    Anti-Inflammatory, Antioxidant and Neuroprotective Effects of Niacin on Mild Traumatic Brain Injury in Rats
    (Turkish Neurosurgical Soc, 2023) Ozaydin, Dilan; Bektasoglu, Pinar Kuru; Koyuncuoglu, Turkan; Ozkaya, Seyma Colakoglu; Koroglu, Ayca Karagoz; Akakin, Dilek; Erzik, Can
    AIM: To study the effects of niacin, a water-soluble vitamin, on inflammation, oxidative stress and apoptotic processes observed after mild traumatic brain injury (TBI).MATERIAL and METHODS: A total of 25 Wistar albino male rats were randomly divided into control (n=9), TBI + Placebo group (n=9), TBI + niacin (500 mg/kg; n=7) groups. Mild TBI was performed under anesthesia by dropping a 300 g weight from a height of 1 meter onto the skull. Behavioral tests were applied before and 24 hours after TBI. Luminol and lucigenin levels and tissue cytokine levels were measured. Histopathological damage was scored in brain tissue.RESULTS: After mild TBI, luminol and lucigenin levels were increased (p<0.001), and their levels were decreased with niacin treatment (p<0.01-p<0.001). An increased score was obtained with trauma in the tail suspension test (p<0.01), showing depressive behavior. The number of entries to arms in Y-maze test were decreased in TBI group compared to pre-traumatic values (p<0.01), while discrimination (p<0.05) and recognition indices (p<0.05) in object recognition test were decreased with trauma, but niacin treatment did not change the outcomes in behavioral tests. Levels of the anti-inflammatory cytokine IL-10 were decreased with trauma, and increased with niacin treatment (p<0.05). The histological damage score was increased with trauma (p<0.001), and decreased with niacin treatment in the cortex (p<0.05), and hippocampal dentate gyrus region (p<0.01).CONCLUSION: Niacin treatment after mild TBI inhibited trauma-induced production of reactive oxygen derivatives and elevated the anti-inflammatory IL-10 level. Niacin treatment ameliorated the histopathologically evident damage.
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    Antioxidant and neuroprotective effects of dexpanthenol in rats induced with traumatic brain injury
    (Elsevier Sci Ltd, 2023) Bektasoglu, Pinar Kuru; Koyuncuoglu, Turkan; Ozaydin, Dilan; Kandemir, Cansu; Akakin, Dilek; Yuksel, Meral; Gurer, Bora
    Trauma-induced primary damage is followed by secondary damage, exacerbating traumatic brain injury (TBI). Dexpanthenol has been shown to protect tissues against oxidative damage in various inflammation models. This study aimed to investigate possible antioxidant and neuroprotective effects of dexpanthenol in TBI. Wistar albino male rats were randomly assigned to control ( n = 16), trauma ( n = 16) and dexpan-thenol (500 mg/kg; n = 14) groups. TBI was induced under anesthesia by dropping a 300 g weight from 70-cm height onto the skulls of the rats. Twenty-four hours after the trauma, the rats were decapitated and myeloperoxidase (MPO) levels, luminol-and lucigenin-enhanced chemiluminescence (CL), malondi-aldehyde (MDA) levels, superoxide dismutase (SOD) levels, and catalase (CAT) and caspase-3 activities were measured in brain tissues. Following transcardiac paraformaldehyde perfusion, histopathological damage was graded on hematoxylin-eosin-stained brain tissues. In the trauma group, MPO level, caspase-3 activity and luminol-lucigenin CL levels were elevated ( p < 0.05-0.001) when compared to controls; meanwhile in the dexpanthenol group these increases were not seen ( p < 0.05-0.001) and MDA levels were decreased ( p < 0.05). Decreased SOD and CAT activities ( p < 0.01) in the vehicle-treated TBI group were increased above control levels in the dexpanthenol group ( p < 0.05-0.001). in the dexpanthenol group there was relatively less neuronal damage observed micro-scopically in the cortices after TBI. Dexpanthenol reduced oxidative damage, suppressed apoptosis by stimulating antioxidant systems and alleviated brain damage caused by TBI. Further experimental and clinical investigations are needed to confirm that dexpanthenol can be administered in the early stages of TBI. (c) 2023 Elsevier Ltd. All rights reserved.
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    SARS-CoV-2 Causes Brain Damage: Therapeutic Intervention with AZD8797
    (Oxford Univ Press, 2023) Demirci, Elif Kervancioglu; Onen, Engin Alp; Yilmaz, Erva Sevic; Koroglu, Ayca Karagoz; Akakin, Dilek
    Elevated CX3CL1 is associated with severe COVID-19 and neurologic symptoms. We aimed to investigate the potential protective effects of selective CX3CR1 antagonist AZD8797 on SARS-CoV-2-induced neuronal damage, and to identify the underlying mechanisms. K18-hACE2 transgenic mice (n = 37) were randomly divided into control groups and SARS-CoV-2 groups, with and without intraperitoneal administration of vehicle or AZD8797 (2.5 mg/mL/day), following exposure to either a single dose of SARS-CoV-2 inhalation or no exposure. Object recognition and hole board tests were performed to assess memory function. Postinfection 8 days, brain tissues were analyzed for histopathological changes, viral, glial, apoptotic, and other immunohistochemical markers, along with measuring malondialdehyde, glutathione, and myeloperoxidase activities. Serum samples were analyzed for proinflammatory cytokines. The SARS-CoV-2 group showed significant weight loss, neuronal damage, oxidative stress, and impaired object recognition memory, while AZD8797 treatment mitigated some of these effects, especially in weight, apoptosis, glutathione, and MCP-1. Histopathological analyses supported the protective effects of AZD8797 against SARS-CoV-2-induced damage. The CX3CL1-CX3CR1 signaling pathway could offer a promising target for reducing SARS-CoV-2's neurological impact, but additional research is needed to confirm these findings in combination with other therapies and assess the clinical significance.