电刺激应激对C57 BL/6小鼠腹腔巨噬细胞产生白细胞介素1的影响

The Effect of Stress with Electric Tail-shock on Interleukin-1 Production by Peritoneal Exudate Macrophage of C57 BL/6 Mice

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 effect of stress with electric tail-shock on interleukin-1 (IL-1) production by peritoneal exudate jnacrophages of C57 BL/6 mice was studied. The results showed that IL-1 level was decreased to 63.7±5.5%, 59.2±4.8%, and 61.2±3.8% of that of control 6 h, 12h, and 20h after stress, respectively (P<0.01). But there were no significant differences in IL-1 level from that of control in 1 h, and 3h tail-shock group. Furthermore, afler macrophages from 6h, 12 h and 20 h stressed mice were incubated in cell culture incubator for 2h, 4h and 8 h, the IL-1 level induced by LPS increased progressively to the level of control. Our findings suggest that stress with electric tail-shock for more than 6h inhibited IL-1 production, and this inhibition was reversible.