|
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 |
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