甲硫氨酸脑啡肽诱导巨噬细胞功能改变。

Met-enkephalin induced alterations of macrophage functions.

作者信息

Fóris G, Medgyesi G A, Gyimesi E, Hauck M

出版信息

Mol Immunol. 1984 Aug;21(8):747-50. doi: 10.1016/0161-5890(84)90029-4.

Abstract

Met-enkephalin /Met-enk/ was found to stimulate IgG2a-mediated antibody dependent cytotoxicity /ADCC/ of thioglycollate elicited rat peritoneal macrophages /PM/ through naloxone-sensitive opiate receptors in concentrations ranging from 10(-9) - 14(-7) M. Phagocytosis of IgG2a coated 51Cr-sheep red blood cell /SRBC/ was suppressed by M-enk in the same concentration range. In the same range of concentrations, M-enk was observed to induce a significant increase in the generation of luminol dependent chemiluminescence /LDCL/. The observed stimulation of ADCC was abolished by calmodulin inhibitor triflouroperazine /TFP/ in 10(-6) M concentration. The involvement of cyclic nucleotides in the M-enk induced functional alterations is indicated by finding cGMP accumulation to be augmented in M-enk treated PMs.

摘要

甲硫氨酸脑啡肽（Met-enkephalin /Met-enk/）被发现可通过纳洛酮敏感的阿片受体，刺激由巯基乙酸诱导的大鼠腹腔巨噬细胞（PM）产生IgG2a介导的抗体依赖性细胞毒性（ADCC），其浓度范围为10^(-9) - 10^(-7) M。在相同浓度范围内，甲硫氨酸脑啡肽（M-enk）抑制了IgG2a包被的51Cr - 绵羊红细胞（SRBC）的吞噬作用。在相同浓度范围内，观察到甲硫氨酸脑啡肽（M-enk）可使鲁米诺依赖性化学发光（LDCL）的产生显著增加。浓度为10^(-6) M的钙调蛋白抑制剂三氟拉嗪（TFP）消除了观察到的ADCC刺激作用。在经甲硫氨酸脑啡肽（M-enk）处理的PM中，发现cGMP积累增加，这表明环核苷酸参与了甲硫氨酸脑啡肽（M-enk）诱导的功能改变。