Alterations by indomethacin in proinflammatory consequences of salivary gland cytosolic phospholipase A2 activation by Porphyromonas gingivalis: Role of leptin

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Abstract

In this study, we report on the alterations by cyclooxygenase inhibitor, indomethacin, in the generation of proinflammatory lipid mediators in sublingual salivary gland acinar cells as a consequence of cytosolic phospholipase A 2 (cPLA2) activation by the lipopolysaccharide (LPS) of a periodontopathic Porphyromonas gingivalis, and assess the role of leptin in the process. We show that indomethacin while not affecting the LPS-induced enhancement in cPLA2-catalyzed arachidonic acid release, caused inhibition in prostaglandin E2 (PGE2) production, up-regulation in apoptosis and platelet activating factor (PAF) generation, and potentiation of the impairment in mucin synthesis. Preincubation with leptin countered the stimulatory effect of indomethacin on the LPS-induced PAF generation and apoptosis, and evoked reduction in the effect of indomethacin on the LPS-induced impairment in mucin. Moreover, the effect of indomethacin on the LPS-induced impairment in mucin synthesis was inhibited by PAF receptor antagonist, BN52020. Our findings demonstrate that indomethacin exacerbates the LPS-induced proinflammatory consequences of cPLA2 activation by causing up-regulation in PAF generation that leads to enhancement in apoptosis and potentiation of the impairment in mucin synthesis. We also show that leptin counters the pathological implications of up-regulation in inflammatory lipid mediators production at the level of cPLA2 activation.

Original languageEnglish (US)
Pages (from-to)127-136
Number of pages10
JournalJournal of Applied Research
Volume7
Issue number1
StatePublished - 2007

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmacology (medical)

Keywords

  • Cytosolic phospholipase A activation
  • Indomethacin
  • Leptin
  • Platelet activating factor
  • Porphyromonas gingivalis
  • Salivary mucin

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