Pharmacological Approaches and Regeneration of Bone Defects with Dental Pulp Stem Cells

Figure 2

NSAID effect on COXs in prostaglandin E2 (PGE2) synthesis and pathways. Arachidonic acid is released from membrane phospholipids by phospholipase A2 and converted into PGH-2 by COXs. Activity of COXs, COX-1 and COX-2, is inhibited by NSAIDs. PGE2 is produced by PGE synthase and signals by binding to its G protein-coupled receptors EP1–EP4. Activation of EP1 (coupled to Gq) increases intracellular Ca2+ via phospholipase C (PLC). Activation of EP3 (coupled to Gi) increases intracellular Ca2+ via PLC and/or inhibits cAMP production via adenylate cyclase (AC). Activation of EP2 or EP4 (both coupled to Gs) stimulates cAMP production via AC. Activation of EP4 also increases protein kinase B (AKT/PKB) via stimulation of phosphoinositide 3-kinase (PI3K). Activation of G protein-coupled receptor triggers many signalling pathways and affects several transcription factors and gene expression levels.