Despite substantial development in medical treatment strategies scientists are struggling to find a cure against spinal cord injury (SCI) which causes long term disability and paralysis. The prime rationale behind it is the enlargement of primary lesion due to an initial trauma to the spinal cord which spreads to the neighbouring spinal tissues It begins from the time of traumatic event happened and extends to hours and even days. It further causes series of biological and functional alterations such as inflammation, excitotoxicity and ischemia, and promotes secondary lesion to the cord which worsens the life of individuals affected by SCI. Oxidative DNA damage is a stern consequence of oxidative stress linked with secondary injury causes oxidative base alterations and strand breaks, which provokes cell death in neurons. It is implausible to stop primary damage however it is credible to halt the secondary lesion and improve the quality of the patient’s life to some extent. Therefore it is crucial to understand the hidden perspectives of cell and molecular biology affecting the pathophysiology of SCI. Thus the focus of the review is to connect the missing links and shed light on the oxidative DNA damages and the functional repair mechanisms, as a consequence of the injury in neurons. The review will also probe the significance of neuroprotective strategies in the present scenario.

The extension of the lesion following spinal cord injury (SCI) poses a major challenge for regenerating axons, which must grow across several centimetres of damaged tissue in the absence of ordered guidance cues. Biofunctionalized electroconducting microfibres (MFs) that provide biochemical signals, as well as electrical and mechanical cues, offer a promising therapeutic approach to help axons overcome this blind journey. We used poly(3,4-ethylenedioxythiophene)-coated carbon MFs functionalized with cell adhesion molecules and growth factors to bridge the spinal cord after a partial unilateral dorsal quadrant lesion (PUDQL) in mice and followed cellular responses by intravital two-photon (2P) imaging through a spinal glass window. Thy1-CFP//LysM-EGFP//CD11c-EYFP triple transgenic reporter animals allowed real time simultaneous monitoring of axons, myeloid cells and microglial cells in the vicinity of the implanted MFs. MF biocompatibility was confirmed by the absence of inflammatory storm after implantation. We found that the sprouting of sensory axons was significantly accelerated by the implantation of functionalized MFs after PUDQL. Their implantation produced better axon alignment compared to random and misrouted axon regeneration that occurred in the absence of MF, with a most striking effect occurring two months after injury. Importantly, we observed differences in the intensity and composition of the innate immune response in comparison to PUDQL-only animals. A significant decrease of immune cell density was found in MF-implanted mice one month after lesion along with a higher ratio of monocyte-derived dendritic cells whose differentiation was accelerated. Therefore, functionalized carbon MFs promote the beneficial immune responses required for neural tissue repair, providing an encouraging strategy for SCI management.