AI Article Synopsis
- The study aimed to determine if increased levels of peripheral corticotropin releasing hormone (CRH) contribute to heightened sensitivity to pain in the abdomen after intestinal inflammation in rats.
- Researchers measured inflammatory markers and pain responses in rats at several time points after inducing colitis, finding that while inflammation subsided, CRH levels and pain responses stayed elevated for a week before normalizing.
- Use of a CRH antagonist reduced the pain sensitivity in inflamed rats, and administering CRH to healthy rats caused similar pain responses, indicating that CRH plays a key role in post-inflammatory pain sensitivity.
Article Abstract
Aim: To investigate whether peripheral corticotropin releasing hormone (CRH), which is up-regulated in intestinal inflammation, mediates the post-inflammatory visceral hypersensitivity in a rat model of colitis.
Methods: We measured mucosal myeloperoxidase (MPO) activity as a marker of inflammation, plasma CRH level, and abdominal withdrawal reflex (AWR) to colorectal distension as a visceral nociceptive response at 2, 7 and 14 d after the induction of colitis with 4% acetic acid.
Results: Colonic inflammation, quantified by MPO activity, significantly increased on d 2 and subsided thereafter, which indicated a resolution of inflammation within 7 d. On the contrary, plasma CRH level and AWR score were increased on d 2, remained high on d 7, and returned to control level on d 14. Intraperitoneal injection of a CRH antagonist, astressin (30 mug/kg), significantly attenuated the post-inflammatory visceral hypersensitivity on d 7. Furthermore, intraperitoneal administration of CRH (3 and 10 mug/kg) mimicked the post-inflammatory visceral hypersensitivity in naive rats.
Conclusion: These results suggest that increased peripheral CRH mediates the enhanced visceral nociception in rats recovered from experimental colitis.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2684000 | PMC |
| http://dx.doi.org/10.3748/wjg.14.731 | DOI Listing |
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