• Rafet Özay, Erhan Türkoğlu, Bora Gürer, Habibullah Dolgun, Oya Evirgen, Berrin İmge Ergüder, Nazlı Hayırlı, Levent Gürses, Zeki Şekerci, and Erdal Reşit Yılmaz.
• Ministry of Health Diskapi Yildirim Beyazit Training and Research Hospital, Neurosurgery Clinic, Ankara, Turkey. Electronic address: rftozay@hotmail.com.
• World Neurosurg. 2017 Jan 1; 97: 407-415.

BackgroundThe development of secondary brain injury via oxidative stress after traumatic brain injury (TBI) is well known. Decorin (DC) inactivates transforming growth factor β1, complement system, and tumor necrosis factor α, which are related to oxidative stress and apoptosis. Consequently, the aim of the present study was to evaluate the role of DC on TBI.MethodsA total of 24 male rats were used and divided into 4 groups as follows; control, trauma, DC, and methylprednisolone (MP). The trauma, DC, and MP groups were subjected to closed-head contusive weight-drop injuries. Rats received treatment with intraperitoneal saline, DC, or MP, respectively. All the animals were killed at the 24th hour after trauma and brain tissues were extracted. The oxidant/antioxidant parameters (malondialdehyde, glutathione peroxidase, superoxide dismutase, and NO) and caspase 3 in the cerebral tissue were analyzed, and histomorphologic evaluation of the cerebral tissue was performed.ResultsLevels of malondialdehyde, NO, and activity of caspase 3 were significantly reduced, and in addition glutathione peroxidase and superoxide dismutase levels were increased in the DC and MP groups compared with the trauma group. The pathology scores and the percentage of degenerated neurons were statistically lower in the DC and MP groups than in the trauma group.ConclusionsThe results of the present study showed that DC inactivates transforming growth factor β1 and protects the brain tissue and neuronal cells after TBI.Copyright © 2016 Elsevier Inc. All rights reserved.

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