It has been shown that, transplantation of human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) decreases the number of activated microglia and inhibits the permeation of immune cells and cellular apoptosis in the brain after ischemic brain injury (Yang et al., 2013; Zhu et al., 2014; Wang et al., 2016). Researchers have shown that the injection of hUCB-MSCs throughout the early stage of ischemic brain injury decreased the IL-1β, IL-6, and TNF-α expression levels in the serum and increased IL-10 expression levels. The significant increase of pro-apoptotic genes such as Bad, Bax, p53, AFAP1, caspase 3, and caspase 9 has been observed after the SCI (Sabapathy et al., 2015). IL-10 can decrease the expression of those genes, oxygen free radicals, and cytokines. Upregulation of IL-1β, IL-6, and TNF-α can initiate neuronal death and improve the synthesis of nitric oxide after injury. IL-1β can improve the intracellular calcium concentration and release neurotropic factors, which can induce neuronal apoptosis. Moreover, TNF-α can induce arachidonic acid metabolite release, which enhance extracellular accumulation of glutamate and generate neurodegenerative toxicity. Glutamate-induced cell death in the CNS contains upregulation of caspase 3 and its activation via a caspase-dependent pathway involves mitochondrial signaling. hUCBSCs decline caspase-3 and -7 activities and are responsible for activation of the Akt pathway and regulation of N-methyl-d-aspartic acid receptors, thereby giving neuroprotection to cortical neurons (Dasari, Veeravalli, et al., 2008). Therefore, hUCBSCs transplantation could provide neuroprotection by regulating the balance of pro- and anti-inflammatory cytokines.