Gülşen İsmail, Ak Hakan, Çölçimen Neşe, Alp Hamit H, Akyol Mehmet E, Demir İsmail, Atalay Tugay, Balahroğlu Ragıp, Rağbetli Murat Ç
Department of Neurosurgery, Yüzüncü Yıl University, School of Medicine, Van, Turkey.
Department of Neurosurgery, Bozok University, School of Medicine, Yozgat, Turkey.
World Neurosurg. 2016 Feb;86:243-9. doi: 10.1016/j.wneu.2015.09.052. Epub 2015 Sep 30.
Traumatic brain injury is a leading cause of morbidity and mortality worldwide. We evaluated the neuroprotective effects of thymoquinone (TQ) in a rat model of traumatic brain injury by using biochemical and histopathologic methods for the first time.
Twenty-four rats were divided into sham (n = 8), trauma (n = 8), and TQ-treated (n = 8) groups. A moderate degree of head trauma was induced with the use of Feeney's falling weight technique, and TQ (5 mg/kg/day) was administered to the TQ-treated group for 7 days. All animals were killed after cardiac perfusion. Brain tissues were extracted immediately after perfusion without damaging the tissues. Biochemical procedures were performed with the serum, and a histopathologic evaluation was performed on the brain tissues. Biochemical experiments included malondialdehyde (MDA), reduced and oxidized coenzyme Q10 analysis, DNA isolation and hydroylazation, and glutathione peroxidase, and superoxide dismutase analyses.
Neuron density in contralateral hippocampal regions (CA1, CA2-3, and CA4) 7 days after the trauma decreased significantly in the trauma and TQ-treated groups, compared with that in the control group. Neuron densities in contralateral hippocampal regions (CA1, CA2-3, and CA4) were greater in the TQ-treated group than in the trauma group. TQ did not increase superoxide dismutase or glutathione peroxidase antioxidant levels. However, TQ decreased the MDA levels.
These results indicate that TQ has a healing effect on neural cells after head injury and this effect is mediated by decreasing MDA levels in the nuclei and mitochondrial membrane of neurons.
创伤性脑损伤是全球发病和死亡的主要原因。我们首次通过生化和组织病理学方法评估了胸腺醌（TQ）在创伤性脑损伤大鼠模型中的神经保护作用。
将24只大鼠分为假手术组（n = 8）、创伤组（n = 8）和TQ治疗组（n = 8）。采用Feeney自由落体技术诱导中度颅脑创伤，并对TQ治疗组给予TQ（5 mg/kg/天），持续7天。所有动物在心脏灌注后处死。灌注后立即提取脑组织，避免损伤组织。对血清进行生化检测，并对脑组织进行组织病理学评估。生化实验包括丙二醛（MDA）、还原型和氧化型辅酶Q10分析、DNA分离和水解、谷胱甘肽过氧化物酶以及超氧化物歧化酶分析。
与对照组相比，创伤组和TQ治疗组在创伤7天后对侧海马区（CA1、CA2 - 3和CA4）的神经元密度显著降低。TQ治疗组对侧海马区（CA1、CA2 - 3和CA4）的神经元密度高于创伤组。TQ并未提高超氧化物歧化酶或谷胱甘肽过氧化物酶的抗氧化水平。然而，TQ降低了MDA水平。
这些结果表明，TQ对头部损伤后的神经细胞具有修复作用，且这种作用是通过降低神经元细胞核和线粒体膜中的MDA水平来介导的。
