Abstract
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.
Highlights
MATERIALS AND METHODSSpinal cord injury (SCI) is one of the most serious conditions that cause limb and trunk dysfunction in countries worldwide
There was no significant difference between these two groups in BBB scores, even 3 days after spinal cord injury (SCI) (Figure 2)
Rat models were the most widely used for in-depth research of physiological and pathological events (Sharif-Alhoseini et al, 2017)
Summary
Spinal cord injury (SCI) is one of the most serious conditions that cause limb and trunk dysfunction in countries worldwide. SCI involves biphasic pathophysiological stages that influence the severity of dysfunction. The pathophysiology of SCI has been continuously investigated, the precise pathogenesis has not yet been fully elucidated. Several studies revealed the pathophysiology of injury, including neuronal inflammation, reactive changes in the glia, oxidative stress, neuronal degeneration and apoptosis (Chen et al, 2018; Lu et al, 2018; Meng et al, 2018). Disturbances in the spinal cord blood flow (SCBF), severely reduced oxygen levels, perfusion defects, hemorrhage, ischemia, and hypoxia have been demonstrated as a focus of post-injury pathophysiological changes of acute SCI (Huo et al, 2019)
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