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应激所致的免疫功能改变的机理认为与神经内分泌和免疫系统双向调节作用有关。鉴于白细胞介素1(IL-1)在这双向环路中的作用,促使研究电刺激应激对C57 BL/6小鼠腹腔巨噬细胞产生IL-1的影响。结果表明:应激6、12、20h后IL-1活性明显抑制,分别是正常活性的63.7±5.5％、59.2±4.8％、61.2±3.8％,P值均<0.01。而应激1、3 h后IL-1活性与正常无明显差异。我们进一步观察到:将应激6、12、20 h后的腹腔巨噬细胞在体外温育2、4、8 h后,再用内毒素诱生,随温育时间延长,巨噬细胞产生IL-1水平逐渐回升,8 h后IL-1活性基本恢复正常。上述结果提示:6 h以上电刺激应激抑制IL-1生成,但这种抑制在培养8 h条件下是可逆的。
The mechanism of stress-induced changes in immune function is thought to be related to the neuroendocrine and bi-directional regulation of the immune system. In view of the role of interleukin-1 (IL-1) in this bidirectional loop, the effect of electrical stimulation on IL-1 production by peritoneal macrophages in C57 BL / 6 mice was investigated. The results showed that IL-1 activity was significantly inhibited at 6, 12 and 20 h after stress, respectively, which were 63.7 ± 5.5%, 59.2 ± 4.8% and 61.2 ± 3.8% of normal activity, respectively, P <0.01. After 1,3 h of stress, IL-1 activity had no significant difference with normal. We further observed: 6,12,20 h after stress peritoneal macrophages incubated in vitro 2,4,8 h, and then induced by endotoxin, with the incubation time, macrophages produce IL -1 levels gradually rose, 8 h after IL-1 activity returned to normal. The above results suggest that electrical stimulation above 6 h can inhibit the production of IL-1, but this inhibition is reversible under the conditions of 8 h culture.