Hasturk Askin Esen, Gokce Emre Cemal, Yilmaz Erdal Resit, Horasanli Bahriye, Evirgen Oya, Hayirli Nazli, Gokturk Hilal, Erguder Imge, Can Belgin
Department of Neurosurgery, Oncology Training and Research Hospital, Ankara, Turkey.
Department of Neurosurgery, Ministry of Health, Diskapi Yildirim Beyazit Education and Research Hospital, Ankara, Turkey.
Asian J Neurosurg. 2018 Oct-Dec;13(4):1018-1025. doi: 10.4103/ajns.AJNS_29_17.
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.
Thirty-six male Wistar albino rats were distributed into three groups ( = 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.
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.
ETA significantly improves neural function and prevents post-TBI histopathological damage in rats.
本研究旨在探讨依那西普(ETA)对大鼠创伤性脑损伤(TBI)后组织病理学和生化变化的影响。
将36只雄性Wistar白化大鼠分为三组(每组 = 12只)。对照组大鼠未遭受创伤。创伤组大鼠仅接受TBI。ETA组大鼠接受TBI加ETA(5 mg/kg腹腔注射[i.p.])。这些组进一步细分为在超急性期(TBI后1小时)处死的组(对照组-1、创伤组-1和ETA组-1)和急性期(TBI后6小时)处死的组(对照组-6、创伤组-6和ETA组-6)。分析肿瘤坏死因子-α、白细胞介素-1β、丙二醛、过氧化氢酶、谷胱甘肽过氧化物酶和超氧化物歧化酶的组织水平。还进行了组织病理学和超微结构评估。
与创伤组相比,在1小时和6小时腹腔注射ETA可显著降低炎性细胞因子表达,减轻氧化应激和脂质过氧化,防止细胞凋亡,并增加抗氧化防御机制活性。与闭合性颅脑损伤创伤组相比,ETA治疗的大鼠组织病理学和超微结构异常显著减少。
ETA可显著改善大鼠神经功能并预防TBI后的组织病理学损伤。