Scientists find new way to treat inflammation pain

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In a new study, researchers found that delta opioid receptors have a built-in mechanism for pain relief and can be precisely targeted with drug-delivering nanoparticles.

This makes them a promising target for treating chronic inflammatory pain with fewer side effects.

The study was done by an international team of researchers.

Opioid receptors—which are primarily located throughout the central nervous system and gut—relieve pain when they are activated by opioids, both those naturally produced by the body and those taken as medications.

While there are several types of opioid receptors, the majority of opioid medications like oxycodone and morphine act on the mu-opioid receptor.

Opioid medications have significant side effects mediated by the mu-opioid receptor, including constipation and difficulty breathing.

These drugs are addictive and their effectiveness diminishes over time, so people require higher doses to manage their pain, leading to increased side effects and risk of overdose.

In this study, the researchers focused on a different opioid receptor: the delta-opioid receptor, which also inhibits pain when activated but offers a promising target for treating pain with fewer side effects.

They conducted experiments using cells from humans and mice with inflammatory bowel disease, which can cause chronic pain.

The researchers discovered that the delta-opioid receptor provides a built-in mechanism to relieve inflammatory pain.

The inflammatory cells from the colon release their own opioids, which activate the delta-opioid receptor and block the activity of neurons in the gut that transmit pain signals.

To target the delta-opioid receptor, the researchers encapsulated a painkiller called DADLE, which binds to the delta-opioid receptor, inside nanoparticles—microscopic vehicles used to deliver drugs to cells.

They then coated the nanoparticles with the same painkiller, which steered the nanoparticles specifically to nerve cells that control pain and away from other cell types, avoiding side effects.

After binding to the receptors of nerve cells, the nanoparticles entered the cells to reach the endosome and then slowly released the painkiller to activate the delta-opioid receptor.

This resulted in a long-lasting activation of the delta-opioid receptor, suggesting a sustained ability to inhibit inflammatory pain.

These findings demonstrate that not only are delta-opioid receptors in endosomes a built-in mechanism for pain control, but also a viable therapeutic target for relief from chronic inflammatory pain.

One author of the study is Nigel Bunnett, Ph.D., professor and chair of the Department of Molecular Pathobiology at New York University (NYU) College of Dentistry.

The study is published in PNAS.

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