He Yuxin, Yan Huiying, Ni Hongbin, Liang Weibang, Jin Wei
Department of Neurosurgery, Drum Tower Clinical Medical College, Nanjing Medical University.
Department of Neurosurgery, Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School, Nanjing, Jiangsu Province, People's Republic of China.
Neuroreport. 2019 Mar 20;30(5):344-349. doi: 10.1097/WNR.0000000000001205.
Secondary brain injury imposes great effects on the prognosis of patients following traumatic brain injury (TBI). Accumulating evidence suggests that nuclear factor erythroid 2-related factor 2 (Nrf2) could play a neuroprotective role in experimental TBI models by regulating the expression of numerous antioxidant, anti-inflammatory, and neuroprotective proteins. However, whether Nrf2 is activated in patients following TBI is still unknown. In this study, human brain tissues were obtained during surgery from patients suffering from TBI. The purpose of this study was to investigate the expression of Nrf2 and Nrf2-regulated gene products, NAD(P)H quinine oxidoreductase 1, and glutathione S-transferase in human injured brain tissue after TBI. Our results revealed that the nuclear level of Nrf2 was significantly increased in injured brain tissues, whereas the cytoplasmic level of Nrf2 was markedly decreased. In addition, the expression of NAD(P)H quinine oxidoreductase 1 and glutathione S-transferase was significantly upregulated. Nrf2 may be activated and confer neuroprotection against secondary brain injury following TBI. Therefore, Nrf2 could serve as a promising molecular target for the treatment of TBI.
继发性脑损伤对创伤性脑损伤(TBI)患者的预后有很大影响。越来越多的证据表明,核因子红细胞2相关因子2(Nrf2)可通过调节多种抗氧化、抗炎和神经保护蛋白的表达,在实验性TBI模型中发挥神经保护作用。然而,TBI患者体内的Nrf2是否被激活仍不清楚。在本研究中,从TBI患者手术过程中获取人脑组织。本研究的目的是调查TBI后人脑损伤组织中Nrf2及其调控的基因产物NAD(P)H醌氧化还原酶1和谷胱甘肽S转移酶的表达情况。我们的结果显示,损伤脑组织中Nrf2的核水平显著升高,而其胞质水平明显降低。此外,NAD(P)H醌氧化还原酶1和谷胱甘肽S转移酶的表达显著上调。Nrf2可能被激活,并对TBI后的继发性脑损伤具有神经保护作用。因此,Nrf2有望成为治疗TBI的分子靶点。