Camphorquinone-induced phospholipase A2 and cyclooxygenase −2 expression and its roles in 8-isoprostane and prostaglandin E2 production of human dental pulp cells

Camphorquinone (CQ) is a widely-used photo-initiator in dentin bonding agent (DBA) and composite resin to promote resin polymerization and restore tooth decay. CQ may potentially induce pulpal inflammation and affect viability of dental pulp especially when the remaining dentin is minimal. Phospholipase A2 (PLA2) and cyclooxygenase-2 (COX-2) are crucial enzymes for tissue inflammation by inducing prostaglandins' production. However, little is known about the PLA2 isoforms’ expression and their response to CQ in the dental pulp. Human dental pulp cells (HDPCs) were exposed to various concentrations of CQ with/without inhibitors (aspirin, eugenol or ASB14780) for 24 h. Protein and mRNA expression of cyclooxygenase-2 (COX-2), cPLA2, sPLA2 and iPLA2 were investigated by immunofluorescent staining and real-time PCR, respectively. Culture medium was collected for analysis of 8-isoprostane and PGE 2 production by enzyme-linked immunosorbant assay. Cell layer was utilized for MTT assay of cell viability. CQ regulated the mRNA and protein expression of COX-2, cPLA2, sPLA2 and iPLA2 at concentrations of 2 and 3 mM. Aspirin, eugenol and ASB14780 (a PLA2 inhibitor) differentially attenuated the CQ-induced PGE 2 production in HDPCs. Aspirin, but not ASB14780 and eugenol, inhibited CQ-induced 8-isoprostane production. On the other hand, eugenol, ASB14780, and aspirin showed little effect on CQ-induced cytotoxicity to HDPCs. CQ may possibly stimulate pulpal inflammation and necrosis by induction of cytotoxicity, 8-isoprostane and PGE2 production that are differentially regulated by various PLA2s. Aspirin, eugenol and PLA2 inhibitors may have potential therapeutic use to control pulpal inflammation after composite resin restoration.