Rafet Özay1, Mehmet Erhan Türkoğlu2, Bora Gürer3, Habibullah Dolgun2, Oya Evirgen4, Berrin İmge Ergüder5, Nazlı Hayırlı4, Levent Gürses2, Zeki Şekerci2. 1. Ministry of Health Diskapi Yildirim Beyazit Training and Research Hospital, Neurosurgery Clinic, Ankara, Turkey. Electronic address: rftozay@hotmail.com. 2. Ministry of Health Diskapi Yildirim Beyazit Training and Research Hospital, Neurosurgery Clinic, Ankara, Turkey. 3. Ministry of Health Fatih Sultan Mehmet Training and Research Hospital, Neurosurgery Clinic, Istanbul, Turkey. 4. Ankara University Faculty of Medicine, Department of Histology and Embryology, Ankara, Turkey. 5. Ankara University Faculty of Medicine, Department of Biochemistry, Ankara, Turkey.
Abstract
BACKGROUND: The 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. METHODS: A 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. RESULTS: Levels 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. CONCLUSIONS: The 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.
BACKGROUND: The 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. METHODS: A 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. RESULTS: Levels 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. CONCLUSIONS: The 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.
Authors: Mohammed Z Nasrullah; Khalid Eljaaly; Thikryat Neamatallah; Usama A Fahmy; Abdulmohsin J Alamoudi; Hussain T Bakhsh; Ashraf B Abdel-Naim Journal: Pharmaceuticals (Basel) Date: 2022-06-23