Zozulia A A, Patsakova E, Kost N V, Ivanushkin A M, Voronkova T L
Biull Eksp Biol Med. 1986 Dec;102(12):731-3.
Beta-endorphin (10(-11)-10(-9) M) has been shown to induce naloxone-independent depression of the proliferative activity of human peripheral lymphocytes (HL), stimulated by pokeweed mitogen without affecting PHA-stimulated HL proliferation. Beta-endorphin (10(-10)-10(-7) M) also caused changes in HL cAMP level, that were blocked by naloxone. Marked individual sensitivity to beta-endorphin effects has been noted. It has been also shown that a bone marrow preparation, stimulating antibody production (myelopeptides), causes naloxone-independent depression in the proliferative activity of HL, stimulated by PHA and pokeweed mitogen, as well as naloxone-blocked decrease in cAMP HL level. It has been concluded that beta-endorphin interacts with several types of opiate lymphocyte receptors and that opioids, contained in myelopeptides, are involved in the realization of myelopeptide effect on lymphocytes.
β-内啡肽(10⁻¹¹ - 10⁻⁹ M)已被证明可诱导人外周淋巴细胞(HL)增殖活性出现纳洛酮非依赖性抑制,此抑制作用由商陆有丝分裂原刺激产生,且不影响PHA刺激的HL增殖。β-内啡肽(10⁻¹⁰ - 10⁻⁷ M)还会引起HL细胞中cAMP水平的变化,这种变化可被纳洛酮阻断。已观察到个体对β-内啡肽效应存在显著敏感性。研究还表明,一种刺激抗体产生的骨髓制剂(骨髓肽)可导致PHA和商陆有丝分裂原刺激的HL增殖活性出现纳洛酮非依赖性抑制,以及HL细胞中cAMP水平出现纳洛酮阻断的降低。由此得出结论,β-内啡肽与多种类型的阿片类淋巴细胞受体相互作用,且骨髓肽中所含的阿片类物质参与了骨髓肽对淋巴细胞作用的实现。