Modulation of Aryl Hydrocarbon Receptor Expression Alleviated Neuropathic Pain in a Chronic Constriction Nerve Injury Animal Model

Neuropathic pain, a persistent condition resulting from somatosensory system damage, affects a significant portion of the population and responds poorly to common analgesics. This study investigates the role of the Aryl hydrocarbon receptor (AhR) in regulating neuropathic pain using nerve explant culture and a chronic constrictive nerve injury (CCI) model in mice. The study found that AhR deletion worsened nerve damage and inflammation, while the AhR agonist omeprazole attenuated these effects. This suggests that AhR agonists could be potential candidates for treating neuropathic pain. Researchers used nerve explants from wild-type and AhR-knockout mice to examine omeprazole's ability to prevent nerve degeneration. They also subjected both types of mice to chronic constrictive nerve injury, treating some with omeprazole, and then analyzed neurobehavior and tissues.

• 1
  Deletion of AhR aggravated nerve damages and this was restored by omeprazole, indicating a protective role of AhR in nerve health.
• 2
  High expression of AhR in the injured nerve was noted after CCI, suggesting that AhR is involved in the response to nerve injury.
• 3
  Omeprazole interacts with the AhR site (Ser36). In the nerve explant culture or CCI model, AhR deletion aggravated nerve degeneration, while AhR restored the nerve damage.