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Drugs for Treatment of Ulcerative Colitis in IBD01:29

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Ulcerative colitis is a chronic inflammatory condition primarily affecting the colon and rectum. The primary drugs used in the treatment of ulcerative colitis are aminosalicylates. They exhibit anti-inflammatory and immunosuppressive properties. They modulate inflammatory mediators and inhibit the activity of nuclear factor κB (NF-κB). Aminosalicylates also reduce inflammation by inhibiting prostaglandin and leukotriene production and decreasing neutrophil chemotaxis and superoxide...
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Glucocorticoids, a class of anti-inflammatory drugs, are pivotal in treating moderate to severe Crohn's disease by inducing remission. They exhibit their anti-inflammatory action by inhibiting the production of inflammatory cytokines such as tumor necrosis factor (TNF)-α, interleukin (IL)-1, and chemokines like IL-8. In addition, they reduce the expression of inflammatory cell adhesion molecules and inhibit gene transcription of nitric oxide synthase, phospholipase A2, cyclooxygenase-2...
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Inflammatory bowel disease, commonly known as IBD, refers to a collection of disorders that lead to persistent inflammation of the gastrointestinal tract. The two types of IBD are ulcerative colitis, which impacts the colon, and Crohn's disease, which can involve any part of the gastrointestinal segment.
Crohn's disease
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CXCL8 chemokine in ulcerative colitis.

Yunfei Zhu1, Shihua Yang2, Nan Zhao1

  • 1College of Traditional Chinese Medicine, Shandong University of Traditional Chinese Medicine, Jinan 250355, PR China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|March 11, 2021
PubMed
Summary

Ulcerative colitis (UC) involves colon inflammation driven by CXCL8. Targeting the CXCL8-CXCR1/2 axis and non-coding RNAs offers potential new therapies for this inflammatory bowel disease.

Keywords:
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Area of Science:

  • Gastroenterology
  • Immunology
  • Molecular Biology

Background:

  • Ulcerative colitis (UC), a key inflammatory bowel disease (IBD), features colon and rectal mucosal inflammation.
  • Clinical signs include abdominal pain, diarrhea, and hematochezia, with unclear pathogenesis involving dysregulated inflammatory molecules.

Purpose of the Study:

  • To analyze the role of the CXCL8-CXCR1/2 axis and non-coding RNAs (ncRNAs) in UC pathogenesis.
  • To review recent therapeutic strategies targeting the CXCL8-CXCR1/2 axis for UC treatment.

Main Methods:

  • Review of signaling pathways (PI3k/Akt, MAPKs, NF-κB) associated with the CXCL8-CXCR1/2 axis in UC.
  • Analysis of specific non-coding RNA (ncRNA) expression profiles in UC patients.

Main Results:

  • CXCL8 is a critical proinflammatory factor in UC pathogenesis.
  • The CXCL8-CXCR1/2 axis engages multiple signaling pathways implicated in UC.
  • Distinct ncRNA expression profiles are observed in UC patients, suggesting their involvement in inflammation.

Conclusions:

  • The CXCL8-CXCR1/2 axis and ncRNAs are significant factors in UC development.
  • Inhibition of the CXCL8-CXCR1/2 axis presents a promising therapeutic avenue for UC.