• Rafet Özay, Mehmet Erhan Türkoğlu, Bora Gürer, Habibullah Dolgun, Oya Evirgen, Berrin İmge Ergüder, Nazlı Hayırlı, Levent Gürses, and Zeki Şekerci.
• Ministry of Health Diskapi Yildirim Beyazit Training and Research Hospital, Neurosurgery Clinic, Ankara, Turkey. Electronic address: rftozay@hotmail.com.
• World Neurosurg. 2017 Aug 1; 104: 634-643.

BackgroundThe development of secondary brain injury via oxidative stress after traumatic brain injury (TBI) is a well-known entity. Consequently, the aim of the present study was to evaluate the role of omeprazole (OM) on rat model of TBI.MethodsA total of 24 male rats were used and divided into 4 groups as follows; control, trauma, OM, and methylprednisolone (MP). The trauma, OM, and MP groups were subjected to closed-head contusive weight-drop injuries. Rats received treatment with saline, OM, or MP, respectively. All the animals were sacrificed at 24 hours after trauma and brain tissues were extracted. The oxidant/antioxidant parameters (malondialdehyde, glutathione peroxidase, superoxide dismutase, nitric oxide) and caspase-3 in the cerebral tissue were analyzed, and histomorphologic evaluation of the cerebral tissue was performed.ResultsLevels of MDA and activity of caspase-3 were significantly reduced in the OM and MP groups compared with the trauma group. Glutathione peroxidase and superoxide dismutase levels were increased both in the OM and MP groups compared with the trauma group. The pathology scores were statistically lower in the OM and MP groups than the trauma group.ConclusionsThe results of the present study showed that OM was as effective as MP in protecting brain from oxidative stress, and apoptosis in the early phase of TBI.Copyright © 2017 Elsevier Inc. All rights reserved.

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