Sacerdote P, Breda M, Barcellini W, Meroni P L, Panerai A E
Department of Pharmacology, University of Milano, Italy.
Peptides. 1991 Nov-Dec;12(6):1353-6. doi: 10.1016/0196-9781(91)90219-f.
Beta-endorphin (BE) and cholecystokinin (CCK) were measured in fresh PBMC isolated from human subjects and rats. The BE and CCK PBMC contents increased significantly with age both in human and rat models. Moreover, polyclonal stimulation induced a significant decrease of BE but not CCK contents in mononuclear cells from human aged subjects. The time course of changes in BE and CCK concentrations observed in fresh and cultured cells from subjects of different ages did not directly correlate to the time course of age-associated impairment of lectin-induced lymphocyte proliferative response and interleukin-2 synthesis. In fact, the lymphocyte functional defects were significantly observed only in the 71-99 year age group, whereas the neuropeptide changes were already evident in the 31-50 age group. Since BE has been shown to participate in the modulation of the immune system, the age-related modifications of PBMC BE could play a role in the immunodepression observed during aging.
在从人类受试者和大鼠中分离出的新鲜外周血单核细胞(PBMC)中测量了β-内啡肽(BE)和胆囊收缩素(CCK)。在人类和大鼠模型中,BE和CCK在PBMC中的含量均随年龄显著增加。此外,多克隆刺激导致老年人类受试者单核细胞中BE含量显著降低,但CCK含量未降低。在来自不同年龄受试者的新鲜细胞和培养细胞中观察到的BE和CCK浓度变化的时间进程与凝集素诱导的淋巴细胞增殖反应和白细胞介素-2合成的年龄相关损伤的时间进程没有直接关联。事实上,仅在71-99岁年龄组中显著观察到淋巴细胞功能缺陷,而神经肽变化在31-50岁年龄组中已经很明显。由于BE已被证明参与免疫系统的调节,PBMC中BE的年龄相关修饰可能在衰老过程中观察到的免疫抑制中起作用。