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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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    Neuroprotective Effects of Niacin on Ischemia/Reperfusion Injury of the Rabbit Spinal Cord
    (Elsevier Science Inc, 2023) Ermutlu, Ilcim; Fesli, Ramazan; Arikok, Ata Turker; Erguder, Berrin Imge; Kertmen, Hayri; Gurer, Bora
    -OBJECTIVE: Previous studies have shown niacin has neuroprotective effects on the central nervous system. However, its specific effect on spinal cord ischemia/ reperfusion injury has not yet been explored. This study aims to evaluate whether niacin can contribute neuro-protective effects on spinal cord ischemia/reperfusion injury. -METHODS: Rabbits were randomized into 4 groups of 8 animals: group I (control), group II (ischemia), group III (30 mg/kg methylprednisolone, intraperitoneal), and group IV (500 mg/kg niacin, intraperitoneal). The rabbits in group IV were premedicated with niacin for 7 days prior to inducing ischemia/reperfusion injury. The control group was subjected only to a laparotomy, while the remaining groups underwent spinal cord ischemia through a 20-minute occlusion of the aorta caudal to the left renal ar-tery. Following the procedure, levels of catalase, malon-dialdehyde, xanthine oxidase, myeloperoxidase, and caspase-3 were analyzed. Ultrastructural, histopatholog-ical, and neurological evaluations were also performed. -RESULTS: Spinal cord ischemia/reperfusion injury resulted in increased levels of xanthine oxidase, malon-dialdehyde, myeloperoxidase, and caspase-3, with a concomitant decrease in catalase levels. Treatment with methylprednisolone and niacin led to decreased levels of xanthine oxidase, malondialdehyde, myeloperoxidase, and caspase-3 and an increase in catalase. Both methylpred-n isolone and niacin treatments demonstrated improve-ments in histopathological, ultrastructural, and neurological assessments. -CONCLUSIONS: Our findings suggest that niacin has antiapoptotic, anti-inflammatory, antioxidant, and neuro-protective effects at least equal to methylprednisolone in ischemia/reperfusion injury of the spinal cord. This study is the first to report the neuroprotective impact of niacin on spinal cord ischemia/reperfusion injury. Further research is warranted to elucidate the role of niacin in this context.
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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.