|
| Study | Function | Mechanism |
|
| Bayat [12] | Antinecroptosis | Downregulating RIP-3, a vitally crucial mediator involved in necroptosis |
| Immune regulation | Downregulating the number of activated microglia and the levels of TNFα |
| Yu-Taeger [16] | Immune regulation | Secretion of cytokines and growth factors |
| Restoring Iba1 expression and the thickness of the processes of striatum-resident microglia |
| Dopaminergic dysfunction repairment | Increasing expression of TH and DARPP-32 protein expressions |
| Elbaz [17] | Immune regulation | Downregulation of TNF-α and FOXP3 levels |
| Secretion of VEGF, which can significantly decrease cytosolic Ca2+concentration, CaN levels, and NFATc4 expression |
| Neurotrophic function | Upregulation of BDNF |
| Antiapoptosis | Regulating the Wnt/β-catenin signaling pathways |
| Ebrahimi [18] | Antioxidative stress-induced cell death | Secreting factors such as GDNF and VEGF, decreasing oxidative stress-induced cell death |
| Rossignol [20] | Neural protection | Secreting BDNF and regulating other NTFs |
| Sadan [23] | Neural protection | Secreting NTFs |
| Moraes [24] | Antiapoptosis | Secreting FGF-2 to activate the PI3K/Akt pathway, which is related to cell survival |
| Lin [25] | Cell proliferation and differentiation | Improving cell proliferation and differentiation, which might be related to chemokine secretion |
| Improve cell migration to the injury | Inducing microglia activation and neuroblasts migration into the QA-lesioned region |
| Improve angiogenic activity | Integrating with the host cells and increasing the levels of laminin, VWF, SDF-1, and the SDF-1 receptor CXCR4 |
| Antiapoptosis | Regulating the expression of p-Erk1/2 and Bax |
| Lee [28] | Antioxidative stress-induced cell death | Increasing the expressions of CREB, PGC-1α, and molecules that defend against ROS |
| Antiapoptosis | Increasing CREB expression, and secreting soluble factors to reduce the levels of N-terminal fragments of mutant huntingtin |
|
