TABLE 1.
The role of curcumin in bone remodeling.
| Cells model | Dosage range | Active concentration | Functions | Signaling pathways/Mechanisms | References |
|---|---|---|---|---|---|
| Curcumin promotes osteogenic differentiation | |||||
| In vitro, MC3T3-E1 cells | 1–2000 nM | 10 nM | Promotes osteoblasts differentiation, proliferation and mineralization | Wnt/β-catenin and Smad signaling pathways | Yamaguchi et al. (2012), Li et al. (2015), Chen et al. (2016b), Bukhari et al. (2019) |
| In vitro, primary osteoblasts | 0.5, 1 and 2 μM | 0.5 μM | |||
| In vitro, MC3T3-E1 cells | 4 μM | 4 μM | Protects osteoblasts from oxidative stress and apoptosis-induced dysfunction | GSK3β-Nrf2 and ERK signaling pathways | Xin et al. (2015), Chen et al. (2016a), Li et al. (2020) |
| In vitro, primary osteoblasts | 0.5, 1 and 2 μM | 0.5 μM | Inhibits the formation of pro-apoptotic proteins and promotes the formation of anti-apoptotic proteins | ||
| Inhibits oxidative stress | |||||
| Curcumin inhibits osteoclast formation | |||||
| In vitro, BMMs induced by RANKL | 0–25 μM | 5 μM | Inhibits osteoclasts differentiation and formation | Akt/NF-κB/NFATc1 and NF-κB signaling pathways | Oh et al. (2008), Hie et al. (2009), Kim et al. (2011), Park et al. (2011), Yamaguchi et al. (2012), Li et al. (2015), Bukhari et al. (2019), Liang et al. (2020b), Yang et al. (2020) |
| In vitro, RAW 264.7 macrophages induced by RANKL | 1–10 μM | 1 μM | |||
| In vitro, RAW 264.7 macrophages induced by RANKL | 4 μM | 4 μM | Prevents osteoclasts formation by reducing oxidative stress | Suppresses MAPK/NFATc1 signaling pathways | Kim et al. (2011), Xin et al. (2015) |
| Inhibits oxidative stress | |||||
| In vitro, BMMs induced by RANKL | 0.4 μM | 0.4 μM | Prevents osteoclasts formation by inhibiting autophagy | Promotes autophagy activity | Ke et al. (2020) |
Abbreviations: Wnt, wingless and int-1; Smad, recombinant mothers against decapentaplegic homolog; GSK-3β, glycogen synthase 3β; Nrf2, nuclear factor-like 2; ERK, extracellular regulated protein kinases; BMMs, bone marrow-derived macrophages; RANKL, nuclear factor receptor activator kappa B ligand; Akt, protein kinase B; NF-κB, nuclear transcription factor-κB; NFATc1, nuclear factor of activated T cells 1; MAPK, mitogen-activated protein kinase pass.