Yamasaki Y, Shimamura O, Kizu A, Nakagawa M, Ijichi H
Life Sci. 1982 Aug 2;31(5):471-8. doi: 10.1016/0024-3205(82)90333-2.
The formaldehyde method was used to examine the interaction of PGE1 with morphine, beta-endorphin and Met-enkephalin on rat mast cells by their effects on IgE-mediated 14C-serotonin release. PGE1 (2x10(-8) -2x10(-5) M) caused a dose-related inhibition of the mediator release 1 min after an antigen challenge, and morphine (3x10(-7) -3x10(-5) M) reversed this PGE1 effect dose-dependently and stereospecifically; naloxone (2x10(-4) M) antagonized this action of morphine. Beta-Endorphin (3x10(-7) -10(-5) M) and Met-enkephalin (3x10(-6) -10(-4) M) mimicked this morphine action dose-dependently and were antagonized by naloxone (2x10(-4) M). These results suggest that morphine and endorphins modulate immunological mediator release from rat mast cells through opioid receptors.
采用甲醛法，通过观察前列腺素E1（PGE1）、吗啡、β-内啡肽和甲硫氨酸脑啡肽对大鼠肥大细胞免疫球蛋白E（IgE）介导的14C-5-羟色胺释放的影响，来检测它们之间的相互作用。抗原攻击1分钟后，PGE1（2×10-8 - 2×10-5M）引起介质释放呈剂量依赖性抑制，吗啡（3×10-7 - 3×10-5M）可剂量依赖性且立体特异性地逆转PGE1的这种作用；纳洛酮（2×10-4M）可拮抗吗啡的这一作用。β-内啡肽（3×10-7 - 10-5M）和甲硫氨酸脑啡肽（3×10-6 - 10-4M）可剂量依赖性地模拟吗啡的这一作用，并被纳洛酮（2×10-4M）拮抗。这些结果表明，吗啡和内啡肽可通过阿片受体调节大鼠肥大细胞免疫介质的释放。
