We were able to show that these 3,4,5-Trimethoxyphenylacetic acid hUC-MSCs have multilineage potential and that, under suitable culture conditions, they are able to transdifferentiate, in vitro, into adipogenic and osteogenic lineages, and neural cells. It is still unknown whether the application of hUC-MSCs can improve the renal function of patients suffering from AKI. Therefore, before beginning clinical trials, it is necessary to investigate this renoprotective effect of hUC-MSCs in a xenogeneic model of AKI. Until now, no studies have examined the application of hUC-MSCs in immunodeficient mice suffering from AKI. One recent study showed that hUC-MSCs improved the renal function of immunocompetent rats suffering from bilateral renal ischemiareperfusion injury. However, the Cinoxacin mechanisms for the beneficial effects shown in this previous study have not yet been elucidated. For example, that study did not investigate the caspase cascade in apoptosis. As we known, there are two major pathways of caspase cascade in apoptosis: the death-receptor pathway, which is mediated by activation of death receptors, and the mitochondrial pathway, which is mediated by noxious stimuli that ultimately lead to mitochondrial injury. The objectives of the present study were to examine the possible therapeutic potential of hUC-MSCs to rescue immunodeficient mice from AKI and to investigate the possible mechanism by which hUC-MSCs may improve renal function in this xenogeneic model. The discrepant results of cytokine levels between this xenogeneic model and other allogeneic models may be due to the different immune statuses of the hosts. It is well known that NOD-SCID mice manifest multiple functional defects of adaptive and innate immunity, including B and T cell deficiency, a functional deficit in NK cells, and impaired macrophage and complement functions. Therefore, there were no significant changes in pro-inflammatory cytokines and anti-inflammatory cytokines in the renal tissues of NOD-SCID mice suffering from FA-induced AKI. However, folic acid could induce the alternation of cell-death gene expression and the generation of oxidative stress, and the renal damage could have occurred at an earlier time point perhaps 6 hours after folic acid administration. Therefore, it is possible that the contribution of chemokines/ cytokines at an earlier time point preceded the deterioration of renal function although we could not detect the significant differences at day 3. Because of this, we will investigate the chemokines/cytokines at earlier time points in the future. Our present study showed that injection of hUC-MSCs improved renal function in NOD-SCID mice suffering from FAinduced AKI, and promoted proliferation and reduced apoptosis of renal tubular cells. These effects are similar to those reported in other xenogeneic studies. For examples, human BM MSCs were found to attenuate AKI induced by cisplatin in an immunodeficient mouse model via decreased apoptosis and increased proliferation of renal tubular cells, although this study did not investigate transdifferentiation or cytokine effects. Later, this study group demonstrated that human cord blood MSCs had a better survival rate than human BM MSCs in cisplatin-treated mice, and the mechanisms for hCBMSCs to improve renal function of cisplatin-induced mice were by reducing apoptosis and by the rising in tubular cell proliferation. Another study showed that hUC-MSCs improved renal function of immunocompetent rats suffering from bilateral renal IRI through increasing the percentage of PCNA-positive renal tubular cells, as well as by decreasing apoptosis of renal tubular cells, and promoting anti-inflammatory mechanisms. Taken together, MSCs derived from human umbilical cord blood and human umbilical cord could improve renal function in animals suffering from AKI.