Table 2.

The mechanism of difference source of MSCs in treatment Inflammatory Bowel Disease.

MSCs source	Model	Type	Pathway	Dosage	Mechanism	Refs
BM-MSCs	C57BL/6 Mice	IBD	i.v.	1×106 cells	Up-regulation of COX2 and the activation of EP4 receptors	Brown et al. (112)
BM-MSCs	C57BL/6 mice	UC	i.p.	2×106 cells	Through suppression of DCs’ inflammatory phenotype through Gal-3	Nikolic et al. (113)
BM-MSCs	BALB/c mice	UC	i.p.	2×106 cells	Promoted M2-like macrophage polarization and relieved inflammatory responses	Cao et al. (114)
BM-MSCs	Wister rats	UC	i.p.	2×106 cells	By reducing the neutrophil infiltration, lipid peroxidation, and proinflammatory cytokine levels	Froushani et al. (115)
hUC-MSCs	Patients	IBD	i.v.	2.3-4.7×107 cells	Accelerate the apoptosis of active inflammatory cells by down-regulating inflammatory mediator production	Hu et al. (116)
hUC-MSCs	KM mice	IBD	i.p.	1.3×106 cells	By regulating the expression of IL-7	Fei et al. (117)
hUC-MSCs	BALB/c mice	IBD	i.p.	1×106 cells	Modulation of immunosuppression by producing PGE2 inducing TLR3 to activate Notch-1 signaling	Qiu et al. (90)
hUC-MSCs	BALB/c mice	IBD	i.v.	n/a	Reduce ubiquitin-protein expression and reduction of NF-κB and mTOR activation	Wu et al. (118)
hUC-MSCs	C57BL/6 mice	IBD	i.p.	3×106 cells	By inhibiting ERK signalling, polarize neutrophils toward the “N2” phenotype.	Wang et al. (119)
GMSCs	C57BL/6J mice	UC	i.v.	2×106 cells	By downregulating the production of inflammatory cytokines by reducing colonic infiltration of inflammatory cells and promoting the generation/activation of Tregs	Zhang et al. (43)
GMSCs	C57BL/6J mice	UC	i.v.	n/a	By modulating inflammatory immune cells via IL-10 signalling	Lu et al. (120)
GMSCs	C57BL/6J mice	UC	i.v.	2×105 cells	By upregulating expression of FAS ligand	Xu et al. (121)
GMSCs	C57BL/6J B6.129P2-Cbstm1Unc/J, and Cbs+/− mice	UC	i.v.	2×105 cells	By Fas/FasL coupling-induced T-cell apoptosis	Yang et al. (94)
GMSCs	C57BL/6J mice	UC	i.v.	1×106 cells	By upregulating expression of FAS ligand	Yu et al. (122)
HA-MSCs	SD rats	IBD	i.v.	1×106 cells	By producing a variety of humoral factors	Miyamoto et al. (123)
HA-MSCs	CD-1 mice	IBD	i.v.	2×106 cells	By increasing the numbers of Lgr51 intestinal stem cells, stimulating intestinal epithelial cell proliferation, and increasing intestinal angiogenesis	Soontararak et al. (124)
AT-MSCs	C57BL/6J mice	IBD	i.p.	2×106 cells	Increased release of TSG-6 and PGE2	Song et al. (125)
AT-MSCs	C57BL/6J mice	IBD	i.p.	1-5×106 cells	Induces an innate immune memory response	Lopez-Santalla et al. (126)
AT-MSCs	SD rats	UC	i.v.	1×107 cells	By suppressing NF-κB signaling pathway	Qi et al. (127)
MSC-CM	Rat	IBD	i.v.	4.5×107 cells	Produced pleiotropic gut trophic factors	Watanabe et al. (128)
iPSC-MSCs	C57BL/6J mice	IBD	i.p.	2×106 cells	Hyaluronan-CD44 interacts with TSG-6 in an Akt-dependent manner	Yang et al. (129)
DF-MSCs	CD patients	CD	i.v.	n/a	By inducing increased numbers of Tregs and reducing CD4+IL22BP T cell ratio	Zibandeh et al. (130)