THE ROLE OF PROSTAGLANDIN E_2 IN THE PATHOGENESIS OF IMMUNOLOGICALLY MEDIATED APLASTIC ANEMIA IN MICE
Wang Xiaolan Li Shunong (Department of Pathophysiology)
This study was designed to measure the FGE2 level in the spleen of aplastic mice and by using indomethacin to elucidate the role of PGE2 in the pathogenesis of murine aplastic anemia. The level of PGE2 in normal control was 23.08 ± 6.56 ng/mg; in lymphocyte transplantation control was 23.16±8.44 ng/mg; in irradiation control was 789.68 ± 129.89 ng/mg and in aplastic mice was 986.4±300.94 ng/mg (RIA assay). The difference between aplastic mice and the control groups was statistically significant (P0.01). The level of PGE2 in aplastic mice reached its peak at day 4 after lymphocyte transplantation. Then there was a slight decrease till moribund. This indicated that there was no negative correlation between the curve of elevated PGE2 and the curve of decreasing bone marrow nucreated cell in aplastic mice. The PGE2 level in irradiation control returned to normal at day 20 after irradiation. To block the synthesis of FGE2, indomethacin at doses 1 and 5 mg/kg per day was administrated for 7 days. The leval of PGE2 in these mice became negligible, but it could not prevent or delay the development of aplastic anemia. These results indicated that elevated PGE2 was an accompaniment of aplastic anemia but not a pathogenic factor in the development of aplastic anemia.