| Autor: |
Hasturk, Askin Esen, Baran, Cagdas, Yilmaz, Erdal Resit, Arikan, Murat, Togral, Guray, Hayirli, Nazli, Erguder, Berrin Imge, Evirgen, Oya |
| Předmět: |
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| Zdroj: |
Asian Journal of Neurosurgery; Jan-Mar2018, Vol. 13 Issue 1, p37-45, 9p |
| Abstrakt: |
Background: 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). Patients and Methods: Fifty-four male Wistar albino rats were randomly assigned into three main groups: The sham, trauma, and ETA group (n = 18 per group). Each of these groups was further divided into three subgroups (n = 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. Results: 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). Conclusion: 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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