The spinal cord injury (SCI) is very common and has poor prognosis (Webb et al., 2010). SCI could cause severe damage to motor, sensory, and autonomic nervous system and their functions which may lead to severe disabilities (Coutts and Keirstead, 2008). The pathophysiology of SCI after the primary trauma has a vital role in the initial structural disruption. In addition, the secondary process includes the cascades of cellular and biological disruptions which can lead to long-term spinal deficits (Dasari et al., 2014). Increased oxidative stress (Fatima et al., 2015), redox transcription factors activity as well as elevated expression of inflammatory mediators play important roles (Popovich and Jones, 2003) in the promotion of the secondary process after the initial injury. SCI results in structural deformation such as degeneration of axons, disruption of neural tissue, neural and glial cell death, and demyelination around the lesion site. Axonal regeneration is inhibited by myelin-associated inhibitors in the central nervous system (CNS; Geoffroy and Zheng, 2014) and formation of astrogliosis (Deng et al., 2011). The extent of intrinsic cell renewal alone (Li and Lepski, 2013), even after application of mitogenic agents such as variety of growth factors, is not sufficient enough for substantial recovery following SCI (Chhabra and Sarda, 2015). So, therapeutic approaches such as exogenous cell transplantation should be considered.