TABLE 4.
PAF restored PrPSc formation to glucosamine-PI-treated ScGT1 cells
Amount of PrPSc in ScGT1 cells treated for 7 days with glucosamine-PI combined with products released after PLA2 activation is shown. The inhibition of PrPSc formation induced by glucosamine-PI was reversed by the addition of PAF receptor agonists (PAF and C-PAF) but not by lyso-PAF, arachidonic acid, or lyso-phospholipids as shown. Values shown are the mean average PrPSc (pg/106 cells) ± S.D., n = 12.
| Treatment 1 | Treatment 2 | PrPSc (pg/106 cells) |
|---|---|---|
| None | None | 9772 ± 314 |
| 1 μm glucosamine-PI | None | <50a |
| 1 μm glucosamine-PI | 1 μm PAF | 11420 ± 658 |
| 1 μm glucosamine-PI | 1 μm C-PAF | 9412 ± 466 |
| 1 μm glucosamine-PI | 1 μm lyso-PAF | <50a |
| 1 μm glucosamine-PI | 10 μm arachidonic acid | <50a |
| 1 μm glucosamine-PI | 10 μm lyso-phosphatidic acid | <50a |
| 1 μm glucosamine-PI | 10 μm lyso-phosphatidylcholine | <50a |
| 1 μm glucosamine-PI | 10 μm lyso-phosphatidylethanolamine | <50a |
a Amount of PrPSc is significantly less than that of vehicle-treated cells (p < 0.01).