New Approach to Pain Relief Discovered
Researchers have found a new method to block pain signals, which could lead to improved treatments for chronic pain conditions.
Every year, around one in five Americans resort to nonsteroidal anti-inflammatory drugs (NSAIDs) for various pains, including headaches, arthritis, sprains, and menstrual cramps.
These medications, known by names like Advil, Aleve, and Motrin, work by blocking the COX-1 and COX-2 receptors that generate prostaglandins. Prostaglandins are present in nearly all body tissues and play a role in causing inflammation in response to pain.
It’s interesting—while reducing inflammation can help alleviate pain, some inflammation is actually necessary for the body’s healing processes. So, when you take an NSAID, yes, pain might decrease, but you’re also dampening the inflammation that your body needs.
However, researchers at NYU Langone Pain Center in New York City have discovered a way to specifically target the receptors that produce prostaglandins without completely wiping out essential inflammation.
In their recent study, they focused on prostaglandin E2 (PGE2) in Schwann cells, which are located in the peripheral nervous system outside the brain. This network of nerves connects the brain and spinal cord to the rest of the body, and Schwann cells have been linked to migraine pain.
The team identified four different receptors for PGE2. Of these, the EP2 receptor was specifically linked to pain, whereas the EP4 receptor was associated with inflammation.
Using some undisclosed pre-clinical drugs on mice, the researchers managed to target just the EP2 receptor, successfully reducing pain without affecting inflammation. Pierangelo Geppetti, one of the study authors, commented, “Inflammation can be beneficial—it’s crucial for repair and restoring function. Suppressing it with NSAIDs might delay healing and recovery from pain. A smarter way to manage prostaglandin-related pain would be to lower pain levels without interfering with the protective aspects of inflammation.”
This discovery arrives amid ongoing debates regarding another pain reliever, acetaminophen. Recently, President Donald Trump controversially linked this drug, marketed as Tylenol, to a potential increase in autism risk when taken during pregnancy, despite a lack of conclusive evidence.
Published Thursday in the journal Nature Communications, the study involved human Schwann cell samples to determine which receptors needed targeting.
The team observed that injecting pre-clinical drugs into mouse models successfully decreased pain levels while leaving inflammation intact. Geppetti mentioned, “We were surprised to find that blocking the EP2 receptor in Schwann cells got rid of prostaglandin-mediated pain, while allowing inflammation to proceed normally. We essentially separated inflammation from pain.”
Should researchers develop drugs that solely target EP2, this could significantly lessen the reliance on NSAIDs. Incredibly, Americans consume about 30 billion doses of these medications annually.
Long-term use of NSAIDs also raises concerns about gastrointestinal and kidney damage. Thus, researchers believe that finding alternatives could mitigate these risks. Prostaglandins are known to produce a protective mucus layer in the stomach, so when NSAIDs indiscriminately target all receptors, this layer might weaken, exposing the stomach to acid and other harmful substances.
NSAIDs also limit blood flow to the gastrointestinal tract, complicating the stomach’s healing process over time, as well as affecting kidney function similarly.
It’s still uncertain which specific drugs the researchers employed for the study or when they might be accessible to the public.
Geppetti added, “Selective EP2 receptor antagonists could be very beneficial. While further research is necessary—especially concerning side effects related to systemic drug delivery—a targeted approach, like injecting directly into a knee joint, looks promising.”
