Scientists at the New York University Research Center showed for the first time that different prostaglandin receptors are responsible for pain and inflammation in different ways. Before the same medicine blocks both processes, as well known, this new strategy can suppress pain independently without disturbing the body's defense. The study was published in Nature Communications.
Prostaglandins are hormone materials that are excreted in the case of injury or infection. They cause inflammation and causes pain. Most of the pain relief, the so-called non-steroidal anti-inflammatory drugs (Ibuprofen, aspirin, etc.) operate, reducing the level of prostaglandin. However, this approach has its shortcomings. Along with pain, inflammation is also suppressed, which can slow down the recovery.
"Inflammation and pain are usually hand in hand on hand." "However, it is an important step towards new treatments without disturbing pain without disturbing inflammation," said Nigel Banet.
The group focused on Prostagland on E2 (PGE2), which is connected with four different receptors. For a long time, it was considered that EP4 receptor is the main culprit of pain. However, new attempts have shown that another receptor, EP2, plays an important role.
When researchers blocked EP2 in traffic cells (which surround the nerves outside the brain, the mice completely eliminated pain reactions, but inflammation continued to develop normally.
"In our surprise, the Blocking of EP2 removed the pain, but the inflammation continued to develop. We have effectively disabled these processes, "added co-author of the study Piererjello Jepettin from Florence University.
The results were confirmed during the attempts on human cells. EP2 Activity activated a signal chain that maintains pain, but they have nothing to do with inflammation. This implies that the receptor can be considered "a vibrant target" for future drugs.
Translation of: Euromedia24.com
