Table 1.

Proteins involved in the therapeutic mechanism of MSCs.

Therapeutic Benefits	Proteins	Mechanisms
Attenuate inflammation through immunomodulation	IL-1, IFN-γ, TNF-α, MCP-1	Decreased pro-inflammatory cytokines to attenuate inflammation [17,18]
	IL-4, IL-10, TNF-β	Increased anti-inflammatory cytokines to attenuate inflammation [17,18]
	PGE2	Mediated the expression of TNF-α and IFN-γ [19]
	HMGB1	Late pro-inflammatory cytokine [20,21]
Release trophic factors to promote therapeutic effects	BDNF	Promoted neurological recovery [22] and directed differentiation of MSCs [7]
	GDNF	Reduced infarct volume [23]
	NGF	Prevented neuron apoptosis and increased neuron proliferation [24]
	VEGF	Induced angiogenesis [25]
	PDGF	Promoted the migration of cells, promoted the growth of primary cortical neurons, inhibited neuroinflammation, and promoted angiogenesis and axon growth [26,27,28]
Induce angiogenesis	Ang1 and tyrosine protein kinase receptor Tie-2	Increased these proteins to increase blood vessel density at the site of vascular injury [29]
	VEGF and VEGF receptor 2 (Flk1)
Proliferate neuroblasts	Axonal growth-associated proteins and axonal growth-inhibiting proteins	Increased axonal growth-associated proteins and decreased axonal growth-inhibiting proteins to promote axonal growth [30]
	Collagen IV and tight junction protein ZO-1	Increased these proteins to decrease BBB disruption and neuronal loss [31,32]
	p53 protein	Reduced the activity of p53 protein to decrease neuron apoptosis [33]
Replace damaged cells	MAP2 and NeuN	Differentiated into new neurons to replace damaged neurons [9]
	GFAP and CNPase	Differentiated into new glial cells to replace damaged glial cells [9]