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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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    Cerebrolysin Amelioration of Spinal Cord Ischemia/ Reperfusion Injury in Rabbit Model
    (Turkish Neurosurgical Soc, 2023) Tonge, Caghan; Bektasoglu, Pinar Kuru; Gulmez, Ahmet; Turkoglu, M. Erhan; Arikok, Ata Turker; Erguder, Berrin Imge; Gurer, Bora
    AIM: To investigate the effects of cerebrolysin on inflammation, oxidative stress, apoptosis, and neurologic recovery in the setting of an experimental rabbit model of spinal cord ischemia/reperfusion injury (SCIRI).MATERIAL and METHODS: Rabbits were randomly divided into five groups: control, ischemia, vehicle, methylprednisolone (30 mg/kg), and cerebrolysin (5 ml/kg) group. The rabbits in the control group underwent only laparotomy; the other groups underwent spinal cord ischemia and reperfusion injury for 20 minutes. Neurologic examination after 24 hours was based on the Modified Tarlov scale. Myeloperoxidase activities, catalase and malondialdehyde levels, and caspase-3 concentrations were determined in serum and tissue samples. Serum xanthine oxidase levels were studied and histopathological and ultrastructural changes were examined. RESULTS: After SCIRI, serum and tissue myeloperoxidase activities, malondialdehyde levels, caspase-3 concentrations, and serum xanthine oxidase activities were increased (p<0.01-0.001). Catalase levels were significantly diminished (p<0.001). Cerebrolysin treatment correlated with reduced myeloperoxidase and xanthine oxidase activities, malondialdehyde levels and caspase-3 concentrations; and with increased catalase levels (p<0.001, for all). The cerebrolysin group showed improved histopathological, ultrastructural, and neurological outcomes.CONCLUSION: For the first time in the literature, the current study reports anti-inflammatory, antioxidant, antiapoptotic, and neuroprotective effects of cerebrolysin in a SCIRI rabbit model.
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    Mildronate Has Ameliorative Effects on the Experimental Ischemia/Reperfusion Injury Model in the Rabbit Spinal Cord
    (Elsevier Science Inc, 2023) Ozaydin, Dilan; Bektasoglu, Pinar Kuru; Ture, Durukan; Bozkurt, Huseyin; Erguder, Berrin Imge; Sargon, Mustafa Fevzi; Arikok, Ata Turker
    -BACKGROUND: Mildronate is a useful anti-ischemic agent and has antiinflammatory, antioxidant, and neuro-protective activities. The aim of this study is to investigate the potential neuroprotective effects of mildronate in the experimental rabbit spinal cord ischemia/reperfusion injury (SCIRI) model. -METHODS: Rabbits were randomized into 5 groups of 8 animals as groups 1 (control), 2 (ischemia), 3 (vehicle), 4 (30 mg/kg methylprednisolone [MP]), and 5 (100 mg/kg mildr-onate). The control group underwent only laparotomy. The other groups have the spinal cord ischemia model by a 20-minute aortic occlusion just caudal to the renal artery. The malondialdehyde and catalase levels and caspase-3, myeloperoxidase, and xanthine oxidase activities were investigated. Neurologic, histopathologic, and ultrastruc-tural evaluations were also performed. -RESULTS: The serum and tissue myeloperoxidase, malondialdehyde, and caspase-3 values of the ischemia and vehicle groups were statistically significantly higher than those of the MP and mildronate groups (P < 0.001). Serum and tissue catalase values of the ischemia and vehicle groups were statistically significantly lower than those of the control, MP, and mildronate groups (P< 0.001). The histopathologic evaluation showed a statistically significantly lower score in the mildronate and MP groups than in the ischemia and vehicle groups (P < 0.001). The modified Tarlov scores of the ischemia and vehicle groups were statistically significantly lower than those of the control, MP, and mildronate groups (P < 0.001).CONCLUSIONS: This study presented the antiin-flammatory, antioxidant, antiapoptotic, and neuroprotective effects of mildronate on SCIRI. Future studies will elucidate its possible use in clinical settings in SCIRI.
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    Surgical Management Thoracolumbar Fractures in Patients with Ankylosing Spondylitis: Technical Note with Case Series
    (Elsevier Science Inc, 2023) Borekci, Ali; Bektasoglu, Pinar Kuru; Ramazanoglu, Ali Fatih; Hazneci, Julide; Gurer, Bora; Hakan, Tayfun; Celikoglu, Erhan
    - OBJECTIVE: Ankylosing spondylitis (AS) is a chronic matic spinal fractures are mostly caused by hyperextension and are unstable. We report the cases of 5 patients with AS surgically treated for thoracolumbar fractures.- METHODS AND RESULTS: We shared our experience of posterior stabilization surgery performed for the treatment of thoracolumbar fractures after traumas such as fallaccident in patients with AS. Patients were all men, and their ages were between 52 and 77 years. The first 3 patients woke up with neurologic deficits and were managed surgically under general anesthesia. We managed the last 2 patients with unilateral short-level stabilization under local anesthesia followed by bilateral long-level stabilization under general anesthesia. No neurologic deterioration was found in the postoperative examination of these 2 patients. We assume that the reason for neurologic deterioration after general anesthesia is the relaxation of muscles. All 3 columns of the spine are affected in patients with AS and the stability is provided by the tone of the muscles around the spine. -CONCLUSIONS: To prevent postoperative neurologic complications after the surgical treatment of traumatic hyperextension thoracic and lumbar fractures in patients with AS, we recommend securing the fracture level with -nilateral short-level stabilization under local anesthesia anesthesia.