Treatment With 2-BFI Attenuated Spinal Cord Injury by Inhibiting Oxidative Stress and Neuronal Apoptosis via the Nrf2 Signaling Pathway

Frontiers in Cellular Neuroscience

Jie Zhu¹  Qin Rui²  Gang Chen³  Haibo Ni⁴  Xiaolong Lin⁵  Weiping Sha⁵  Huilin Yang⁶  Di Li⁷ 

[1] Department of Anesthesiology, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, China;Department of Laboratory, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, China;Department of Neurosurgery and Brain and Nerve Research Laboratory, The First Affiliated Hospital of Soochow University, Suzhou, China;Department of Neurosurgery, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, China;Department of Orthopaedic Surgery, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, China;Department of Orthopaedic Surgery, The First Affiliated Hospital of Soochow University, Suzhou, China;Department of Translational Medicine Center, The Affiliated Zhangjiagang Hospital of Soochow University, Zhangjiagang, China;

关键词: 2-BFI;    Nrf2;    HO-1;    spinal cord injury;    neuroprotection;   

DOI  :  10.3389/fncel.2019.00567

来源: DOAJ

【 摘 要 】

Previous reports showed that 2-(-2-benzofuranyl)-2-imidazoline (2-BFI) has antioxidant, anti-inflammatory and anti-apoptotic effects on neuroprotection in numerous disorders. However, the precise mechanisms remain elusive. The nuclear factor c factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway plays an important and essential role in the antioxidant and anti-inflammatory responses of the cell. Therefore, the purpose of this study was to investigate the potential neuroprotective effects of 2-BFI in a rat model of spinal cord injury (SCI) and to determine whether its neuroprotective effects are associated with the activation of Nrf2. To test this hypothesis, we examined the potential roles of 2-BFI in SCI models which were established in rats using a clip-compression injury method. Our results showed that treatment with 2-BFI twice daily improved locomotion recovery from SCI, which increased Nrf2 expression in both neurons and astrocytes, meanwhile, the level of heme oxygenase-1 (HO-1) also significantly enhanced. In addition, after the treatment with 2-BFI increased levels of superoxidase dismutase (SOD) and glutathione peroxidase (GPx) indicated the antioxidant effect of the drug. Furthermore, the upregulation of Bcl-2 and downregulation of Bax and caspase-3 implied antiapoptotic effects on neuroprotection of 2-BFI, which were verified by the Fluoro-Jade B (FJB) staining and TUNEL staining. Collectively, these results add to a growing body of evidence supporting that 2-BFI may attenuate SCI mediated by activation of the Nrf2/HO-1 signaling pathway.

【 授权许可】

Unknown