INTRODUCTION: An emerging technology using human embryonic stem cells (hESCs) to 
regenerate infarcted heart tissue has been underdeveloped. However, because 
non-steroidal anti-inflammatory drugs (NSAIDs), such as aspirin, are taken 
during the infarction, it becomes critical to know whether the NSAIDs have 
negative impacts on heart tissue regeneration when using hESCs.
METHODS: Mass spectrometry (LC/MS/MS) and high performance liquid chromatography 
(HPLC) analyses were used to analyze the functional presence of the elaborate 
prostanoids' biosynthesis and signaling systems in hESCs. The detected 
endogenous arachidonic acid (AA) released in the hESC membranes reflects the 
activity of phospholipase which directly controls the biosyntheses of the 
prostanoids.
RESULTS: The complete inhibition of the endogenous prostaglandin E(2) (PGE(2)) 
biosynthesis by the cyclooxygenase-2 (COX-2) inhibitor, NS398, confirmed that 
the major prostanoids synthesized in the hESCs are mediated by the COX-2 enzyme. 
We also found that PGE(2) and the prostacyclin (PGI(2)) metabolite, 
6-keto-PGF(1α), are present in the undifferentiated hESCs.
CONCLUSION: This indicated different cyclooxygenase (COX)-downstream synthases 
and metabolizing enzymes are involved in the AA products' signaling through the 
COX-1 and COX-2 pathways. The presence of many enzymes' and receptors' [(COX-1, 
COX-2, microsomal prostaglandin E synthase (mPGES), cytosolic prostaglandin E 
synthase (cPGES), prostaglandin I synthase (PGIS), the PGE(2) subtype receptors 
(EP(1), EP(2), and EP(4)) and the prostacyclin receptor (IP)] involvement in the 
prostanoid biosynthesis and activity was confirmed by western blot. The studies 
implied the negative effects of NSAIDs, such as aspirin and COX-2 inhibitors, 
which suppress prostanoid production during tissue regeneration for infarcted 
heart when using hESCs.