CC BY-NC-ND 4.0 · Asian J Neurosurg 2018; 13(04): 1018-1025
DOI: 10.4103/ajns.AJNS_29_17
Original Article

Therapeutic evaluation of tumor necrosis factor-alpha antagonist etanercept against traumatic brain injury in rats: Ultrastructural, pathological, and biochemical analyses

Askin Hasturk
Department of Neurosurgery, Oncology Training and Research Hospital, Ankara
,
Emre Gokce
Department of Neurosurgery, Oncology Training and Research Hospital, Ankara
,
Erdal Yilmaz
1   Department of Neurosurgery, Ministry of Health, Diskapi Yildirim Beyazit Education and Research Hospital, Ankara
,
Bahriye Horasanli
2   Department of Neurology, Baskent University Faculty of Medicine, Konya
,
Oya Evirgen
3   Department of Histology and Embryology, Ankara University Faculty of Medicine, Ankara
,
Nazli Hayirli
3   Department of Histology and Embryology, Ankara University Faculty of Medicine, Ankara
,
Hilal Gokturk
4   Department of Histology and Embryology, Yildirim Beyazit University Faculty of Medicine, Ankara
,
Imge Erguder
5   Department of Biochemistry, Ankara University Faculty of Medicine, Ankara
,
Belgin Can
3   Department of Histology and Embryology, Ankara University Faculty of Medicine, Ankara
› Author Affiliations

Purpose: The aim of the present study was to investigate the effect of etanercept (ETA) on histopathological and biochemical changes after traumatic brain injury (TBI) in rats. Materials and Methods: Thirty-six male Wistar albino rats were distributed into three groups (n = 12 each). Control group rats were not subjected to trauma. Trauma group rats were subjected to TBI only. ETA group rats were subjected to TBI plus ETA (5 mg/kg intraperitoneal [i.p.]). The groups were further subdivided into those sacrificed in the hyperacute stage (1 h after TBI) (control-1, trauma-1, and ETA-1 groups) and the acute stage (6 h after TBI) (control-6, trauma-6, and ETA-6 groups). Tissue levels of tumour necrosis factor-alpha, interleukin-1 beta, malondialdehyde, catalase, glutathione peroxidase, and superoxide dismutase were analyzed. Histopathological and ultrastructural evaluations were also performed. Results: i.p. administration of ETA at 1 and 6 h significantly reduced inflammatory cytokine expression, attenuated oxidative stress and lipid peroxidation, prevented apoptosis, and increased antioxidant defense mechanism activity in comparison to trauma group. Histopathological and ultrastructural abnormalities were significantly reduced in ETA-treated rats compared to closed head injury trauma groups. Conclusions: ETA significantly improves neural function and prevents post-TBI histopathological damage in rats.



Publication History

Article published online:
14 September 2022

© 2018. Asian Congress of Neurological Surgeons. This is an open access article published by Thieme under the terms of the Creative Commons Attribution-NonDerivative-NonCommercial License, permitting copying and reproduction so long as the original work is given appropriate credit. Contents may not be used for commercial purposes, or adapted, remixed, transformed or built upon. (https://creativecommons.org/licenses/by-nc-nd/4.0/)

Thieme Medical and Scientific Publishers Pvt. Ltd.
A-12, 2nd Floor, Sector 2, Noida-201301 UP, India