PubMed İndeksli Açık & Kapalı Erişimli Yayınlar
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Item The effects of focal brain damage on fracture healing: An experimental rat study(2019) Arik, Mustafa; Ekinci, Yakup; Gurbuz, Kaan; Batin, Sabri; 31650924Objectives: This study aims to investigate whether the motor cortex (MC) or the somatosensory cortex (SC) is more active during the course of bone healing after traumatic brain injury (TBI). Materials and methods: Thirty-three male Wistar albino rats (age, 8 to 10 months; weighing, 250 to 300 g) were randomized into three groups as the control group, MC damage group and SC damage group. Two rats from each brain damage group were sacrificed to verify the locations of the cortical injuries. Callus formation, callus/diaphysis ratios, and serum alkaline phosphatase (ALP) levels were measured at one, three and six weeks. Results: The increases in callus masses in the control, MC, and SC groups were statistically significantly different between one and three weeks (p<0.05). Although this increase in the MC and SC groups was significant compared to the control group at the end of one week, no statistically significant difference was found between the MC and SC groups (p>0.05). There was a statistically significant difference in callus/diaphysis ratio between control, MC and SC groups in favor of MC group only at one week (p<0.05). The increase in serum ALP levels at three weeks was statistically significantly different in the MC and SC groups compared to the control group and significantly higher in the MC group compared to the SC group (p<0.05). Conclusion: There is a possible relationship between enhanced fracture healing after TBI and damage in the MC. Motor cortex plays a more active role on fracture healing in TBI.Item Therapeutic evaluation of interleukin 1-beta antagonist Anakinra against traumatic brain injury in rats(2015) Hasturk, Askin Esen; Yilmaz, Erdal Resit; Turkoglu, Erhan; Kertmen, Hayri; Horasanli, Bahriye; Hayirli, Nazli; Erguder, Imge Berrin; Evirgen, Oya; 25779705BACKGROUND: The aim of this study was to evaluate the therapeutic efficiency of Anakinra, an IL-1 beta antagonist with anti-inflammatory effects, in an experimental model of traumatic brain injury (TBI). METHODS: Fifty-four rats underwent TBI after a weighted object was dropped onto a metal disc secured to their skulls. Animals were randomized into 3 main groups: control (n=18), TBI + saline (n=18; six animals per time-point) with samples obtained at the first, sixth and twenty-fourth h postoperatively, and TBI + Anakinra (n=18; six animals per time-point) with brain samples obtained at the first, sixth and twenty-fourth h postoperatively. Brain tissue and blood serum were extracted for the analysis of IL-1 beta, malondialdehyde, glutathione peroxidase, superoxide dismutase, and catalase levels. Tissue sections were evaluated histopathologically under a light microscope. RESULTS: After trauma, tissue and serum IL-1 beta levels were significantly elevated and after Anakinra administration, these levels substantially decreased. Glutathione peroxidase, superoxide dismutase, and catalase activity decreased following TBI and Anakinra administration proved effective in increasing the activity of these antioxidant enzymes. Histopathological analysis confirmed that Anakinra might protect the brain tissue and nerve cells from injury. CONCLUSION: Results demonstrate that Anakinra reduces the development of inflammation and tissue injury events associated with TBI.