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Related Experiment Videos

Evidence for a colonic PAF receptor

W E Longo1, J D Carter, B Chandel

  • 1Surgical Research Institute, St. Louis University School of Medicine, Missouri 63110.

The Journal of Surgical Research
|January 1, 1995
PubMed
Summary

Platelet-activating factor (PAF) significantly increases prostanoid release in rabbit colons, causing tissue injury. A PAF antagonist, WEB-2170, blocked this release and reduced injury, indicating a role for PAF receptors in colonic inflammation.

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Area of Science:

  • Gastroenterology
  • Pharmacology
  • Inflammation Research

Background:

  • Platelet-activating factor (PAF) is a potent inflammatory mediator.
  • Eicosanoids play a crucial role in inflammatory processes within the gastrointestinal tract.

Purpose of the Study:

  • To investigate the impact of exogenous platelet-activating factor (PAF) on eicosanoid release from the rabbit left colon.
  • To determine the efficacy of PAF antagonists in blocking PAF-induced eicosanoid release and subsequent tissue injury.

Main Methods:

  • Isolated buffer-perfused rabbit left colon preparation.
  • Infusion of PAF (1.0 or 5.0 µg) into the inferior mesenteric artery.
  • Measurement of prostaglandin E, 6-ketoprostaglandin F1α, thromboxane B2, and leukotriene B4 (LTB4) in venous and luminal effluents using ELISA.

Related Experiment Videos

  • Administration of PAF antagonists (WEB-2170 or alprazolam) prior to PAF infusion.

    • Main Results:

    • PAF infusion significantly increased prostanoid levels in venous and luminal effluents compared to controls.
    • Leukotriene B4 (LTB4) levels were not significantly affected by PAF.
    • WEB-2170, but not alprazolam, effectively blocked PAF-induced prostanoid release.
    • WEB-2170 pretreatment significantly reduced PAF-induced colonic tissue injury.

    Conclusions:

    • A PAF-sensitive receptor is present in rabbit colonic tissue.
    • PAF stimulates prostanoid release, contributing to colonic tissue injury.
    • WEB-2170 demonstrates potential as a therapeutic agent by inhibiting PAF-mediated inflammatory responses in the colon.