Burstein S H, Hull K, Hunter S A, Shilstone J
Department of Biochemistry, University of Massachusetts Medical School, Worcester 01655.
Mol Pharmacol. 1989 Jan;35(1):6-9.
Immunization of mice with a thyroglobulin-prostaglandin E2 (PGE2) conjugate produced animals with measurable blood levels of anti-PGE2 antibodies. When these mice were challenged with delta 1-tetrahydrocannabinol (THC) (20 mg/kg), they showed a greatly diminished cataleptic response as compared with control animals. This observation further supports a hypothesis on the mechanism of action of THC in which eicosanoids, such as PGE2, are early mediators. Based on the likelihood that antibodies were not present in the central nervous system, it is suggested that the initial site of action of THC may be at one or more peripheral locations. The transport of peripheral PGE2 or other eicosanoids to the brain would result in the eventual manifestation of THC action at this site.
用甲状腺球蛋白 - 前列腺素E2(PGE2)偶联物免疫小鼠,所产生的动物体内可检测到抗PGE2抗体的血药浓度。当用δ1 - 四氢大麻酚(THC)(20毫克/千克)对这些小鼠进行激发试验时,与对照动物相比,它们的僵住反应大大减弱。这一观察结果进一步支持了关于THC作用机制的假说,即类花生酸如PGE2是早期介质。基于中枢神经系统中不存在抗体的可能性,提示THC的初始作用部位可能在一个或多个外周部位。外周PGE2或其他类花生酸向脑内的转运将导致THC在此部位作用的最终显现。