The study showed that analgesia mediated by inhibitors of soluble epoxide hydrolase is dependent on a pain-mediating second messenger called cyclic adenosinemonophosphate — or cAMP.
The researchers found that stabilization of natural epoxy-fatty acids through inhibition of sEH reduces pain. However, in the absence of an underlying painful state, inhibition of sEH is ineffective. Surprisingly, a pain-mediating second messenger, cAMP, interacts with natural EFAs and regulates the analgesic activity of sEH inhibitors.
cAMP interacts with natural EFAs to regulate the analgesic or pain activity of sEH inhibitors. Concurrent inhibition of sEH and PDE dramatically reduced acute pain in rodents, according to the study.
Read the abstract on the study in PNAS.
Read more on pain:
–Changes to Epidural Doses Allow Movement Without Pain
–Florida’s Pill Mill Regulations Get More Complicated
–Southeast Pain Care Opens New Location With Stanly Regional Medical Center
