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Apoptotic efficacy and inhibitory effect of dexamethasone on matrix metalloproteinase

Farshid Saadat1, Mohammad Reza Khorramizadeh, Abbas Mirshafiey

  • 1Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.

Medical Science Monitor : International Medical Journal of Experimental and Clinical Research
|July 2, 2005
PubMed
Abstract

Insights

Dexamethasone demonstrated apoptosis induction and matrix metalloproteinase 2 (MMP-2) suppression, suggesting its potential for chemoprevention. Nonsteroidal anti-inflammatory drugs (NSAIDs) showed greater MMP-2 inhibition but induced more apoptosis.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Cell Biology

Background:

  • Matrix metalloproteinases (MMPs) and apoptosis are implicated in inflammatory processes.
  • This study investigates the effects of dexamethasone, piroxicam, and diclofenac on MMP-2 activity and apoptosis.

Purpose of the Study:

  • To compare the effects of dexamethasone with NSAIDs (piroxicam, diclofenac) on apoptosis and MMP-2 activity.
  • To evaluate the potential chemopreventive role of dexamethasone.

Main Methods:

  • Utilized a fibrosarcoma (WEHI-164) cell line for tolerability, MMP-2 activity, and apoptosis assessments.
  • Administered dexamethasone, piroxicam, and diclofenac at varying concentrations (10-200 microg/ml).
  • Assessed MMP-2 activity via zymography and apoptosis using terminal deoxyribonucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL).

Main Results:

  • Dexamethasone exhibited better tolerability than diclofenac at 10-100 microg/ml.
  • NSAIDs showed a more potent dose-dependent inhibition of MMP-2 activity compared to dexamethasone at 10-80 microg/ml.
  • Dexamethasone induced 20.92% apoptosis, compared to 78% for diclofenac and 28.15% for piroxicam.

Conclusions:

  • Dexamethasone effectively induces apoptosis and suppresses MMP-2 activity.
  • Dexamethasone shows promise as a chemopreventive agent.
  • NSAIDs were more effective at inhibiting MMP-2 but induced higher rates of apoptosis.

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