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采用侧脑室注射（ｉｃｖ）孤啡肽（ＯｒｐｈａｎｉｎＦＱ，简称ＯＦＱ）和反义核苷酸（ＡＳＯ）的技术，观察了ＯＦＱ对手术创伤应激介导的自然杀伤细胞（ＮＫ细胞）活性下降效应的影响，结果表明：正常大鼠ｉｃｖＯＦＱ０．１μｇ（０．０５５ｎｍｏｌ）和１．０μｇ（０．５５０ｎｍｏｌ）ＮＫ细胞活性与生理盐水组相比无明显差异。５．０μｇ（２．７５０ｎｍｏｌ）明显抑制正常ＮＫ细胞活性（Ｐ＜０．０５），手术创伤后大鼠的ＮＫ细胞活性明显低于正常对照组（Ｐ＜０．００１）。０．１μｇ、１．０μｇ和５．０μｇ的孤啡肽（ｉｃｖ）均能明显地拮抗由创伤导致的ＮＫ细胞活性抑制（Ｐ＜０．０５），采用ＡＳＯ技术阻断ＯＦＱ的合成后，再给予ＯＦＱ（１．０μｇ，ｉｃｖ）对创伤大鼠的免疫低下效应无影响。研究提示脑内ＯＦＱ在调整创伤应激介导的免疫低下效应中起重要的作用。
To investigate the effect of OFQ on the reduction of natural killer (NK) cell activity induced by traumatic stress in trauma induced by intracerebroventricular injection (icv) of OrphaninFQ (OFQ) and antisense nucleotide (ASO) The results showed that there was no significant difference in the activity of icvOFQ 0.1μg (0.055nmol) and 1.0μg (0.550nmol) NK cells in normal rats compared with the saline group. 5.0μg (2.750nmol) significantly inhibited the activity of normal NK cells (P <0.05). The activity of NK cells in the traumatic rats was significantly lower than that in the normal control group (P <0.001). 0.1μg, 1.0μg and 5.0μg of orphanin (icv) all could obviously antagonize the inhibition of NK cell activity induced by trauma (P <0.05), and blocked the synthesis of OFQ by ASO technology Administration of OFQ (1.0 μg, icv) had no effect on the immunodeficient effect in traumatized rats. Research suggests that OFQ in the brain plays an important role in modulating the effects of traumatic stress-mediated immunodeficiency.