Shibata Y, Ogura N, Moriya Y, Abiko Y, Izumi H, Takiguchi H
Departments of Biochemistry, Nihon University School of Dentistry, Chiba, Japan.
Life Sci. 1991;49(15):1103-9. doi: 10.1016/0024-3205(91)90598-6.
We found that platelet-activating factor (PAF) stimulated the production of prostaglandin (PG) E2 in MC3T3-E1 cells in a time- and dose-dependent manner. 1.0 microM PAF gave a maximal stimulation of PGE2 production by MC3T3-E1 cells after a 4 hr PAF-treatment. Furthermore, the PAF-induced PGE2 production was abolished by the pre-treatment of the cells with a PAF receptor antagonist, 1-O-hexadecyl-2-acetyl-sn-glycero-3-phospho(N,N,N-trimethyl)hexanolamine, which occupied the same receptor site as PAF. These results suggest that PAF stimulates the PGE2 synthesis through a PAF receptor mediated pathway. Possibly PAF modulates bone metabolism by stimulating PGE2 synthesis.
我们发现血小板活化因子(PAF)以时间和剂量依赖的方式刺激MC3T3-E1细胞中前列腺素(PG)E2的产生。在PAF处理4小时后,1.0微摩尔PAF对MC3T3-E1细胞产生的PGE2有最大刺激作用。此外,用PAF受体拮抗剂1-O-十六烷基-2-乙酰基-sn-甘油-3-磷酸(N,N,N-三甲基)己醇胺预处理细胞后,PAF诱导的PGE2产生被消除,该拮抗剂与PAF占据相同的受体位点。这些结果表明,PAF通过PAF受体介导的途径刺激PGE2合成。PAF可能通过刺激PGE2合成来调节骨代谢。