Chulalongkorn University Dental Journal

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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.



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