Osteogenic Differentiation of Mesenchymal Stem Cells via Curcumin-Containing Nanoscaffolds

Table 1

The protocols of curcumin use in cell culture in several signaling pathways.

Signaling pathway	Treatment time	Concentration	Cells	Results	Ref
Akt-GSK3β	9 h	50 μM	Human osteoblastic cell line (Saos-2)	(i) Curcumin was cytoprotective since it significantly improved the viability of cells exposed to H2O2 and reduced H2O2-induced apoptosis.; (ii) Curcumin preserved the potential of mitochondrial redox, reduced the mitochondrial oxidative status, and improved the mitochondrial membrane potential and functions.; (iii) Curcumin increased of phosphorylated glycogen synthase kinase-3β (GSK3β) and phosphorylated protein kinase B (Akt) levels.	[22]
Wnt/TCF and Wnt/β-catenin	24 h	50 or 100 μM	Human aMSCs	(i) Curcumin protects from cell death caused by H2O2.; (ii) Curcumin increased the osteoblast differentiation that is inhibited by H2O2.; (iii) Curcumin attenuated the oxidative stress and the inhibition of Wnt/β-catenin signaling.; (iv) Curcumin can indorse osteoblast differentiation and protect the inhibitory effect elicited by oxidative injury.	[23]
PI3K/AKT/Nrf2	7 days	0.1 μM	Periodontal ligament stem cells	(i) A suitable concentration of curcumin had no cytotoxicity and could indorse osteogenic differentiation.; (ii) Curcumin can stimulate the osteogenesis, and the influence is related to the PI3K/AKT/Nrf2 signaling pathway.	[24]
ER stress	1, 3, 7, or 15 days	10 μM	C3H10T1/2 mesenchymal cells	(i) Curcumin exhibited no cytotoxic activity at concentrations up to 10 μM. Curcumin-induced mild ER stress increases differentiation of osteoblast by ATF6 expression in C3H10T1/2 cells.	[20]
GSK3β-Nrf2	7 days	0.25 μM	MC3T3-E1 cells	(i) GSK3β-Nrf2 activation and ROS scavenging can be the key responsible mechanism for prosurvival and differentiation-stimulating actions of curcumin in H2O2-induced oxidative damage of MC3T3-E1 cells.	[25]