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Related Experiment Videos

Ketoprofen-induced intestinal permeability changes studied in side-by-side diffusion cells.

Igor Legen1, Albin Kristl

  • 1Faculty of Pharmacy, University of Ljubljana, Askerceva 7, 1000 Ljubljana, Slovenia.

The Journal of Pharmacy and Pharmacology
|October 25, 2002
PubMed
Summary

Non-steroidal anti-inflammatory drugs (NSAIDs) like ketoprofen increase intestinal permeability. Lower doses disrupt prostaglandin control of tight junctions, while higher doses cause energy depletion, both increasing gut permeability.

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Area of Science:

  • Gastroenterology
  • Pharmacology
  • Cell Biology

Background:

  • Non-steroidal anti-inflammatory drugs (NSAIDs) are known to increase intestinal permeability.
  • This increase is hypothesized to stem from tight junction disruption due to reduced prostaglandin synthesis or cellular energy depletion.
  • Understanding these mechanisms is crucial for managing NSAID-induced gastrointestinal side effects.

Purpose of the Study:

  • To investigate the precise mechanisms by which ketoprofen affects intestinal permeability in rat jejunum.
  • To differentiate the roles of prostaglandin synthesis inhibition and energy depletion in NSAID-induced gut barrier dysfunction.
  • To correlate ketoprofen concentration with specific changes in intestinal electrical and transport properties.

Main Methods:

Related Experiment Videos

  • In vitro assessment of rat jejunum using electrical parameters: tissue electrical resistance (TER), short circuit current (I(sc)), and transepithelial potential difference (PD).
  • Measurement of paracellular marker (fluorescein) transport across the jejunum.
  • Comparison of ketoprofen effects with a known metabolic inhibitor, sodium azide.

    • Main Results:

    • Ketoprofen significantly increased fluorescein transport and decreased TER in a concentration-dependent manner.
    • At lower concentrations (< 5 mM), ketoprofen affected TER and fluorescein transport but not I(sc) or D-glucose transport.
    • At higher concentrations, ketoprofen reduced I(sc) and D-glucose transport, similar to sodium azide, while markedly increasing fluorescein transport.

    Conclusions:

    • At lower concentrations, ketoprofen-induced intestinal hyperpermeability is likely due to impaired prostaglandin-mediated tight junction regulation.
    • At higher concentrations, ketoprofen appears to increase intestinal permeability primarily through ATP depletion, impairing cellular energy-dependent functions.
    • These findings elucidate distinct concentration-dependent mechanisms of NSAID-induced intestinal damage.