This research was hinged on the promotion of the therapeutic properties of hUCBSCs in combination with a neuroprotective agent to induce curative effects to SCI in rats. The present study demonstrated that combination of MO extract and hUCBSCs transplantation has neuroprotective properties in treatment of SCI. Although this combination promoted the motor, sensory, and EMG functions, there were no significant differences between SCI-MO, SCI-hUCBSCs, and SCI-MO-hUCBSC groups. A number of previous investigations have revealed functional improvement after transplantation of hUCBSCs in SCI (Saporta et al., 2003; Kuh et al., 2005; Dasari, Spomar, et al., 2008; Rodrigues et al., 2012). Previous research has shown that administration of MO extract itself improved neurological and cellular outcomes in rat SCI (Hosseini et al., 2015). MO has neuroprotective and neurotrophic effects, including promotion of functional recovery, thereby suggesting that it has therapeutic effect on neurodegenerative diseases (Bayat et al., 2012; Sepand et al., 2013). MO has acetylcholinesterase inhibitory properties (Dastmalchi et al., 2009). Anticholinesterases increase the residence time of acetylcholine in the synapse. This allows rebinding of the transmitter to nicotinic receptors. It thus gives acetylcholine the competitive advantage over the neuromuscular blocking agent (Nair and Hunter, 2004). Our results revealed that the combination of hUCBSCs and MO prevented cell loss, formation of cavity, and astrogliosis in ventral horn and also enhances the myelination in the dorsal white matter of spinal cord after injury. The effect of hUCBSCs and MO on enhancing functional recovery, myelination, and reducing astrogliosis and cavity formation is likely attributable to the inhibition of pro-inflammatory cytokines. Inflammatory processes have fundamental roles in the pathophysiology of SCI. Pro-inflammatory cytokines, including IL-1 and TNF-α, are released by activation of neurons, astrocytes, microglia, and endothelial cells after injury. Thereafter, the secondary inflammatory response and activation of IL-6 and IL-8 are induced by those cytokines (Zhu et al., 2014).