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Table 1 MT is an effective agent to alleviate the apoptotic factors for protecting MSCs from injury, while it also acts as an inhibitory agent or a promotive agent according to MSC differentiation fate

From: Melatonin plays critical role in mesenchymal stem cell-based regenerative medicine in vitro and in vivo

Concentration Time point MSC resource Effect Mechanism Ref
10 nM, 1 μM, 100 μM Cotreatment Bone marrow No effect on the proliferation of MSCs, inhibits adipogenic differentiation of MSCs, enhances MSC osteogenic differentiation PPARc expression↓, Runx2 expression↑ [49]
50 nM Cotreatment Adipose Increases the ALP expression MT2 receptor↑, MEK/ERK (1/2) ↑ [50]
10 nM, 1 μM, 100 μM Cotreatment Synovium Improves the proliferation of MSCs, protects cell viability in the presence of IL-1β, promotes MSC osteogenic differentiation when exposed to IL-1β SOD↑ [52]
1 μM, 10 μM, 100 μM Cotreatment Adipose Reduces the senescent progress and abnormal activation of autophagy AKT↑, ROS↓ [53]
50 μM, 100 μM Post-treatment Bone marrow Reduces cell death of MSCs AMPK↑, acetyl-CoA carboxylase↑ [54]
1 μM Pretreatment Adipose Enhances MSC proliferation and self-renewal and diminishes the extent of MSC apoptosis PrPC-dependent pathway↑ [55]
10–300 nM Pretreatment Bone marrow Protects against hypoxia/serum deprivation-induced injury ERK1/2↑ [56]
5 μM Pretreatment Bone marrow Prevents MSC apoptosis Mitogenic factors↑ [57]
10 nM, 1 μM, 100 μM Post-treatment Bone marrow Reverses H2O2-induced senescence P38MAPK↓, p16INK4α↓, SIRT1↑ [59]
10 nM, 1 μM, 100 μM Post-treatment Bone marrow Restores the impaired differentiation ability of MSCs induced by H2O2 SIRT1↑ [59]
10 nM, 1 μM, 100 μM Pretreatment Bone marrow Maintains the morphology, viability, and osteogenic differentiation ability of MSCs ROS↓, p53/ERK/p38↓ [61]
50 nM Cotreatment Bone marrow Inhibits adipogenic differentiation of MSCs at the early stage of adipogenic differentiation ROS↓, phosphorylating ERK/GSK-3β↓ [62]
50 nM Cotreatment Bone marrow Promotes chondrogenic differentiation of MSCs MT receptor-dependent pathway↑ [63]
50 nM Cotreatment Bone marrow Restores the pellet size and matrix accumulation, upregulates chondrogenic differentiation of MSCs, reduces cell apoptosis during the whole chondrogenesis IL-1β-induced activation of NF-κB signaling↓ [64]
1 μM Cotreatment Synovium Rescues the IL-1β and TNF-α impaired chondrogenesis of MSCs ROS↓, SOD↑, MMPs↓ [65]
10 μM, 50 μM, 100 μM, 200 μM Pretreatment Adipose Rescues MSCs from cell death induced by oxidative stress; 100 μM of MT confers greater cytoprotection on MSCs than 200 μM ROS↓, P38MAPK↓, harmful inflammatory cytokines↓