Dong Nan, Diao Yi, Ding Maohua, Cao Baoqiang, Jiang Dehua
Department of Neurosurgery, Xuzhou Central Hospital, Xuzhou, Jiangsu 221009, P.R. China.
Exp Ther Med. 2017 Jun;13(6):3183-3188. doi: 10.3892/etm.2017.4411. Epub 2017 Apr 28.
We investigated the possible role of 7-nitroindazole (7-NI) in regulating serum neuron-specific enolase (NSE) and S100β levels in a rat model of traumatic brain injury (TBI). We also explored the possible mechanism by which 7-NI may affect the level of NSE and S100β. A total of 160 healthy adult male Sprague-Dawley rats were randomly divided into 2 groups: i) The saline-treated group and ii) the 7-NI-treated group. Using the random number table, the groups were further divided into four subgroups: i) The sham-injured group; ii) the TBI 6 h group; iii) the TBI 12 h group; and iv) the TBI 24 h group (n=20). Controlled cortical impact in rats was established. Serum NSE and S100β levels, nitric oxide (NO) level, water content, Evans blue (EB) content, malondialdehyde (MDA) level and total superoxide dismutase (T-SOD) level in the brain tissue were measured. NO synthase (NOS) activity was measured at 6, 12 and 24 h after TBI. Pathological changes in brain tissue were studied by hematoxylin and eosin (H&E) staining at each time-point. NSE and S100β levels, NO content, water content, EB content and MDA level in the brain tissue increased significantly after TBI. NOS activity was also increased significantly after TBI while T-SOD content in brain tissue was significantly reduced after TBI. H&E staining showed that brain damage was aggravated gradually after TBI. We concluded that the early application of 7-NI significantly reduced serum NSE and S100β levels after TBI. The neuroprotective effects of 7-NI may be associated with reduced NOS activity, reduced NO content, alleviated brain edema, lower blood-brain barrier permeability and oxidative stress. Serum NSE and S100β levels can reflect the therapeutic effect of 7-NI, which suggest a good diagnostic value.
我们在创伤性脑损伤（TBI）大鼠模型中研究了7-硝基吲唑（7-NI）在调节血清神经元特异性烯醇化酶（NSE）和S100β水平方面的可能作用。我们还探讨了7-NI可能影响NSE和S100β水平的潜在机制。总共160只健康成年雄性Sprague-Dawley大鼠被随机分为2组：i）生理盐水处理组和ii）7-NI处理组。使用随机数字表，将每组进一步分为四个亚组：i）假损伤组；ii）TBI 6小时组；iii）TBI 12小时组；和iv）TBI 24小时组（n = 20）。建立大鼠控制性皮质撞击模型。测量血清NSE和S100β水平、一氧化氮（NO）水平、含水量、伊文思蓝（EB）含量、丙二醛（MDA）水平以及脑组织中的总超氧化物歧化酶（T-SOD）水平。在TBI后6、12和24小时测量一氧化氮合酶（NOS）活性。在每个时间点通过苏木精和伊红（H&E）染色研究脑组织的病理变化。TBI后，脑组织中的NSE和S100β水平、NO含量、含水量、EB含量和MDA水平显著升高。TBI后NOS活性也显著增加，而脑组织中的T-SOD含量在TBI后显著降低。H&E染色显示TBI后脑损伤逐渐加重。我们得出结论，TBI后早期应用7-NI可显著降低血清NSE和S100β水平。7-NI的神经保护作用可能与降低NOS活性、降低NO含量、减轻脑水肿、降低血脑屏障通透性和氧化应激有关。血清NSE和S100β水平可反映7-NI的治疗效果，具有良好的诊断价值。
