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. 2016 Aug 25;14(4):3620–3626. doi: 10.3892/mmr.2016.5674

Figure 4.

Figure 4

Curcumin inhibits the osteoclastogenic potential of PBMCs from patients with RA. (A) PBMCs from healthy controls were incubated with various concentrations of curcumin (0–40 µM) in the presence of M-CSF (50 ng/ml) and RANKL (100 ng/ml) for 48 h, and the cell viability was examined using the Cell Counting kit-8 assay. Cell viability was not affected by <20 µM curcumin. PBMCs from patients with RA were incubated with various concentrations of curcumin (0–10 µM) in the presence of 50 ng/ml M-CSF and 100 ng/ml RANKL for 14 days. (B) The osteoclast differentiation was measured by TRAP staining and the number of osteoclasts (TRAP-positive cells containing ≥3 nuclei/cell) was counted in 10 fields of each sample. Curcumin treatment inhibited the number of osteoclasts generated in a dose-dependent manner. The (C) mRNA and (D) protein expression levels of RANK were measured by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively, and were reduced by curcumin treatment. (E) The protein expression levels of (E) c-Fos and NFATc1, and (F) p-ERK1/2, ERK1/2, p-p38, P-38, p-JNK and JNK were measured and normalized to β-actin. Curcumin treatment decreased the protein expression levels of c-Fos, NFATc1, p-ERK1/2, p-p38 and p-JNK in a dose-dependent manner. Data are expressed as the mean ± standard deviation, n=3 per group. *P<0.05, **P<0.01 and ***P<0.001 vs. 0 µmol/l curcumin treatment. PBMCs, peripheral blood mononuclear cells; M-CSF, macrophage colony-stimulating factor; RANKL, receptor activator of nuclear factor κB ligand; RA, rheumatoid arthritis; RANK, receptor activator of nuclear factor κB; TRAP, tartrate-resistant acid phosphatase; NFATc1, nuclear factor of activated T cells, cytoplasmic 1; p, phosphorylated; ERK1/2, extracellular signal-regulated kinases 1 and 2; JNK, c-Jun N-terminal kinase.