白细胞介素－2中枢镇痛作用途径的探讨

POSSIBLE MECHANISM OF THE ANALGESIC EFFSCT OF INTERLEUKIN-2 IN CENTRAL NERVOUS SYSTEM

抗ＩＬ－２受体α亚基的单克隆抗体不能阻断ＩＬ－２的中枢镇痛作用，以及丧失与ＩＬ－２受体β亚基结合能力的ＩＬ－２突变体仍具有提高大鼠痛阈的能力，这表明ＩＬ－２的中枢镇痛作用并不是通过ＩＬ－２受体所介导，亦表示ＩＬ－２的免疫和镇痛作用是通过不同的受体途径实现的。加之内源性阿片肽与ＩＬ－２分子有着共同的抗原决定基和结构相似性，提示ＩＬ－２可以与阿片受体直接结合产生中枢镇痛效应。从放射免疫法测定的ＩＬ－２侧脑室注射后不同时间大鼠脑内不同核团的内源性阿片肽含量，推测ＩＬ－２的中枢镇痛作用可能还与弓状核、室旁核、蓝斑等核团的β－ＥＰ和ＬＥＫ有关。

The monoclonal antibody against IL-2R (Tao) could not block the analgesic effect of IL-2, and IL-2 mutant that could not bind to β subunit of IL-2 receptor still had capabilityof increasing the pain threshold of rats. All these facts suggest that the analgesiceffect of IL-2 in CNS is not mediated through the IL-2 receptor, and that the immuneand analgesic effects of IL-2 are mediated through different receptor mechanisms. It is suggested that there are common antigenic determinants and similar structurebetween IL-2 and endogenous opioid peptides (EOP). This implies that the analgesic effect of IL-2 might be mediated by interaction between IL-2 and opioid receptors in CNS. Using radioimmunoassay the contents of EOP of different nuclei were measured at different times after injecting IL-2 into the lateral ventricle of rats. The results suggested that the analgesic effect of IL-2 may be related to β-EP and LEK in arcuate hypothalamic nucleus, paraventricular hypothalamic nucleus and locus ceruleus.