• Varittha Thongtan, D.D.S., M.Sc., Dip. Thai Board of Pediatric Dentistry
• Supaporn Suttamanatwong, D.D.S., Certificate in Orthodontics, Ph.D.

Background Prostaglandin E2 (PGE2) is the main mediator for receptor activator of nuclear factor-κB
ligand (RANKL)-mediated osteoclastogenesis and bone resorption in periodontitis. Bone marrow
stromal cells (BMSCs) secrete PGE2 in response to pro-inflammatory cytokines, such as tumor
necrosis factor-alpha (TNF-α). Curcumin, a polyphenolic compound from the turmeric plant,
possesses an anti-inflammatory effect by downregulating key mediators of inflammation.

Objectives This study examined the effect of curcumin on the process of PGE2 biosynthesis in
TNF-α-stimulated BMSCs.

Materials and methods To investigate curcumin cytotoxicity, mouse ST2 BMSCs were treated with
1-50 μM curcumin and cell viability was determined by the MTT assay. Next, BMSCs were treated
with curcumin for 30 minutes followed by TNF-α stimulation. The level of PGE2 in the culture media
and the expression of cyclooxygenase (COX)-2 and microsomal prostaglandin E synthase (mPGES)-1
was measured using enzyme-linked immunosorbent assay (ELISA) and quantitative polymerase chain
reaction, respectively.

Results One to ten μM curcumin promoted cell viability, whereas 30-50 μM curcumin was cytotoxic.
TNF-α dose-and time-dependently upregulated COX-2 expression, showing the highest increase by
20 ng/mL at 24 hours. Curcumin (10-20 μM) significantly reduced TNF-α-stimulated COX-2
expression. Curcumin (20 μM) almost completely inhibited the TNF-α-induced PGE2 synthesis.
Although mPGES-1 expression was also upregulated by TNF-α, it was not affected by curcumin
treatment.

Conclusion Curcumin enhanced cell viability and inhibited TNF-α-induced PGE2 synthesis in ST2
BMSCs via COX-2, but not mPGES-1, suppression. These findings suggest a therapeutic potential of
curcumin for inflammation-induced bone diseases and tissue regeneration.

(CU Dent J. 2017;40:13-26)