| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1988: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1987: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
The aim of the present research program was to determine whether platelet-activating factor (PAF) was produced in dental pulp tissue and to evaluate the possible role of PAF in pulp inflammatory process. At first, the bioassay system for the detection of PAF was established by using rabbit washed platelets. This bioassay system enabled us to detect as low as 2.5 pg PAF in an aggregation assay tube. Dental pulp tissues isolated from rat incisors were incubated for 30 min with or without 10 m calcium ionophore A23187. Lipids were extracted and purified by thin layer chromatography, and the platelet-aggregating activity was determined. A23187 stimulation, although slightly, induced the production of platelet-aggregating activity. This sggregating activity was identified as PAF by several criteria. However, neither acetyl CoA nor PMSF, known as stimulants of PAF biosynthesis, increased A23187-induced PAF production. Further, neither thrombin nor histamine induced PAF production by the pulp tissue, whereas these substances stimulated PAF production by human vascular endothelial cells in culture.
When [^3H]PAF was incubated with pulp tissue, PAF was metabolized to lyso PAF and acyl PFC. On the other hand, when dental pulp tissue was stimulated by PAF, the production of prostaglandin (PF) L_2 and thromboxane (TX) A_2 was stimulated. This stimulatory effect was inhibited by the several specific antagonists although the PAF receptor subtype mediating PGL_2 and TXA_2 production seemed to be different. The precise mechanism of the stimulatory effect may be also different between the two metabolites in terms of the dependency on calcium ions. These findings suggest that PAF may be produced and has important roles by interacting with arachidonate metabolites in the pulp inflammatory process. The in vivo study using pulp inflammatory model would be required to confirm the precise roles of PAF in the inflammation of the bental pulp.
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