| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
Inflammatory cytokines seem to play important roles in neointima formation and affects the origin of cells. On the injured vessel surface, mural thrombus release various cytokines from activated platelets or leukocytes included in it. In the present study, we have investigated the effect of inflammatory cytokines and inflammatory disease, on platelet activation as follows :
1)Syrian Hamster (8 weeks old, male) was anaesthetized with sodium pentobarbital (64mg/kg, i.p.) and blood was collected from inferior vena cava. Platelet aggregation was measured by whole blood aggregation using counting method, or by Platelet Rich Plasma aggregation using light transmission method. As results ; (1)Interleukin-8 (IL-8) alone slightly induced whole blood aggregation in hamster blood. (2)On the other hand, IL-8 did not induce platelet aggregation in PRP, nor enhanced ADP-induced aggregation. From these results, IL-8 seems to stimulate leukocyte or erythrocyte in whole blood, and indirectly activate platelet.
2)Inflammatory Bowel Disease model mouse was prepared, by adding 4% dextran sodium sulfate (DSS) in the drinking water of ICR mouse (5 weeks old male). Using blood of this model animal, we have measure platelet aggregation by the same method as described above. DSS loading have enhanced Adenosine DiPhosphate-induced PRP aggregation. These results suggest that inflammation would modulate platelet activity, in the early stage as 1 week.
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