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ATP-induced histamine release is in part related to Phospholipase A2- mediated arachidonic acid metabolism in rat peritoneal mast cells

  • Yun Hye Lee
  • Seung Jun Lee
  • Moo Hyun Seo
  • Chang Jong Kim
  • Sang Soo Sim
Research Article Pharmacology, Toxicology & Pharmaceutics

Abstract

Histamine and arachidonic acid (AA) release was measured using the P2-purinoceptor antagonists, phospholipase A2 (PLA2) and cyclooxygenase (COX)/lipoxygenase (LOX) inhibitors to determine whether or not ATP-induced histamine release is associated with arachidonic acid (AA) release in rat peritoneal mast cells. ATP increased histamine release in a dose dependent manner, whereas adenosine did not. PPADS (a selective P2X-purinoceptor antagonist) and suramin (a nonselective P2X,2Y-purinoceptor antagonist) inhibited ATP-induced histamine release in a dose dependent manner. However, RB-2 (a P2Y-purinoceptor antagonist) did not block ATP-induced histamine release. Manoalide and oleyloxyethyl phosphorylcholine (OPC), secretory PLA2 inhibitors, also inhibited ATP-induced histamine release dose-dependently. Both COX inhibitors (ibuprofen and indomethacin) and LOX inhibitors (baicalein and caffeic acid) inhibited ATP-induced histamine in a dose dependent manner. ATP significantly increased [3H]AA release by 54%. PPADS and suramin significantly inhibited ATP-induced [3H]AA release by 81% and 39%, respectively. ATP-induced histamine release was significantly inhibited by a variety of protein kinase inhibitors, such as bisindolmaleimide, genistein, methyl 2,5-dihydroxycinnamate, W-7 and trifluoperazine. Overall, the results suggest that ATP-induced histamine release is in part related to the PLA2-mediated AA metabolism and P2X-purinoceptors.

Key words

ATP Arachidonic acid Purinoceptor Histamine Mast cells 

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Copyright information

© The Pharmaceutical Society of Korea 2001

Authors and Affiliations

  • Yun Hye Lee
    • 1
  • Seung Jun Lee
    • 1
  • Moo Hyun Seo
    • 1
  • Chang Jong Kim
    • 1
  • Sang Soo Sim
    • 1
  1. 1.Department of Pathophysiology, College of PharmacyChung-Ang UniversitySeoulKorea

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