| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1993: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Research Abstract |
1.We have investigated the immunosuppressive effect of 16,16-dimethyl prostaglandin E2 (DMPGE2) in rat cardiac allotransplantation model. Intragraft delivery of DMPGE2 for 14 day completely inhibited refection of LEW cardiac allograft in BUF recipients. To further evaluate the responsible mechanisms for DMPGE2 induced tolerance, we have characterized the participating cell types and the kinetics of the leukocyte influx during the first 96 hr after syngeneic BUF of allogeneic LEW renal transplantation in BUF recipients. Intragraft infusion of DMPGE2 markedly inhibited the monocyte influx into the renal interstitium, but not the glomeruli, of allografts, while demonstrating relatively little effect on the migration of leukocytes into the renal glomerulus or renal interstitium of isografts. These results suggest that inhibition of leukocyte accumulation into the renal allograft might be one of the possible mechanisms responsible for DMPGE2 induced immunosuppressive effect.
2.Donor treatment with gadolinium chloride (GD) significantly improved recipient survival after transplantation of 12 hr cold stored livers in rats. Isolated Kupffer cells (KC) from GD treated livers showed dramatically reduced TNF production compared to control group. PGE2 production by KC in GD group was, however, comparable to that for control group. Although these results suggest that PGE2 released from KC has little impact on TNF production by KC,addition of DMPGE2 might reduce TNF production. We are also currently investigating the cytoprotective effect of GD and DMPGE2 on warm ischemia induced liver damage in rats.
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