Hasturk Askin Esen, Baran Cagdas, Yilmaz Erdal Resit, Arikan Murat, Togral Guray, Hayirli Nazli, Erguder Berrin Imge, Evirgen Oya
Department of Neurosurgery, Oncology Training and Research Hospital, Ankara, Turkey.
Department of Cardiovascular Surgery, Ankara University Faculty of Medicine, Ankara, Turkey.
Asian J Neurosurg. 2018 Jan-Mar;13(1):37-45. doi: 10.4103/ajns.AJNS_307_16.
The aim of our study is to assess the neuroprotective effects of the tumor necrosis factor alpha (TNF-α) inhibitor etanercept (ETA) on histopathological and biochemical changes following spinal cord injury (SCI).
Fifty-four male Wistar albino rats were randomly assigned into three main groups: The sham, trauma, and ETA group ( = 18 per group). Each of these groups was further divided into three subgroups ( = 6 per subgroup) based on the different tissue sampling times postinjury: 1 h, 6 h, and 24 h. Clip compression model was used for SCI. Rats in the ETA group were treated with 5 mg/kg of ETA immediately after the clip was removed. After 1, 6, and 24 h, the spinal cord was totally removed between the levels T8-T10. Sample tissue was immediately harvested and fixed for histopathological and electron microscopic examination and were analyzed for TNF-α, interleukin-1β (IL-1β), superoxide dismutase (SOD), adenosine deaminase, catalase (CAT), and malondialdehyde levels in both the tissue and serum.
The serum and tissue levels of cytokines and enzymes were seen to change after SCI between hyperacute, acute, and subacute stages. Treatment with ETA selectively inhibited TNF-α, and IL-1β expression together with increased levels of antioxidative enzymes (SOD, CAT).
Early administration of ETA after SCI may remarkably attenuate neuronal injury by decreasing tissue and serum TNF-α and IL-1β levels, while increasing antioxidative enzymes such as SOD and CAT in subacute and acute stages, respectively.
我们研究的目的是评估肿瘤坏死因子α(TNF-α)抑制剂依那西普(ETA)对脊髓损伤(SCI)后组织病理学和生化变化的神经保护作用。
54只雄性Wistar白化大鼠被随机分为三个主要组:假手术组、创伤组和ETA组(每组 = 18只)。根据损伤后不同的组织采样时间,每组又进一步分为三个亚组(每个亚组 = 6只):1小时、6小时和24小时。采用夹闭压迫模型造成脊髓损伤。ETA组大鼠在移除夹子后立即用5mg/kg的ETA进行治疗。在1、6和24小时后,在T8 - T10水平之间完全切除脊髓。立即采集样本组织并固定,用于组织病理学和电子显微镜检查,并分析组织和血清中的TNF-α、白细胞介素-1β(IL-1β)、超氧化物歧化酶(SOD)、腺苷脱氨酶、过氧化氢酶(CAT)和丙二醛水平。
脊髓损伤后,在超急性期、急性期和亚急性期,细胞因子和酶的血清和组织水平发生了变化。ETA治疗选择性地抑制了TNF-α和IL-1β的表达,同时抗氧化酶(SOD、CAT)水平升高。
脊髓损伤后早期给予ETA可通过降低组织和血清TNF-α和IL-1β水平,同时分别在亚急性期和急性期增加抗氧化酶如SOD和CAT的水平,显著减轻神经元损伤。