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电足部电击和心理应激对小鼠脾脏自然杀伤细胞、淋巴因子激活的杀伤细胞、细胞毒性T淋巴细胞、自然杀伤受体以及颗粒酶和穿孔素mRNA转录物活性的影响。

Effect of electric foot shock and psychological stress on activities of murine splenic natural killer and lymphokine-activated killer cells, cytotoxic T lymphocytes, natural killer receptors and mRNA transcripts for granzymes and perforin.

作者信息

Li Qing, Liang Zaifu, Nakadai Ari, Kawada Tomoyuki

机构信息

Department of Hygiene and Public Health, Nippon Medical School, 1-1-5 Sendagi, Bunkyo-ku, Tokyo, 113-8602, Japan.

出版信息

Stress. 2005 Jun;8(2):107-16. doi: 10.1080/10253890500140972.

DOI:10.1080/10253890500140972
PMID:16019602
Abstract

To explore the mechanism of stress-induced inhibition of natural killer (NK) activity, female C57BL/6 mice were stimulated by electric foot shock and psychological stress for 7 days consecutively. The shocked mice received scrambled, uncontrollable, inescapable 0.6 mA electric shocks in a communication box 120 times during 60 min. The mice in the psychological stress group were put into the communication box without electric foot shock. The plasma corticosterone level in both stressed groups was significantly higher than that in controls on days 1, 3, 5 and 7 and showed the highest level on day 3 in the foot shock stress. According to these results, therefore, we investigated the effect of stress on immunological function on day 3, and measured body weight, weight of the spleen, number of splenocytes, splenic NK, lymphokine-activated killer (LAK) and cytotoxic T lymphocyte (CTL) activities, NK receptors, and mRNA transcripts for granzymes A and B and perforin in splenocytes. The NK, LAK and CTL activities, and NK receptors in mice with both types of stress were significantly decreased compared to those of the control mice, but the decreases were greater in the foot-shocked mice than in the psychological-stress mice. The mRNA transcripts for granzyme A and perforin were significantly decreased only in the foot-shocked mice. On the other hand, the foot-shock stress increased granzyme B. The above findings suggest that stress induced inhibition of NK, LAK and CTL activities partially via affecting NK receptors, granzymes and perforin.

摘要

为探究应激诱导的自然杀伤(NK)细胞活性抑制机制,对雌性C57BL/6小鼠连续7天施加电足部电击和心理应激刺激。受电击的小鼠在一个交流箱中于60分钟内接受120次强度为0.6 mA的无序、不可控、无法逃避的电击。心理应激组的小鼠被放入无电足部电击的交流箱中。在第1、3、5和7天,两个应激组的血浆皮质酮水平均显著高于对照组,且在足部电击应激组中第3天达到最高水平。因此,根据这些结果,我们在第3天研究了应激对免疫功能的影响,并测量了体重、脾脏重量、脾细胞数量、脾脏NK细胞、淋巴因子激活的杀伤(LAK)细胞和细胞毒性T淋巴细胞(CTL)活性、NK受体以及脾细胞中颗粒酶A和B及穿孔素的mRNA转录本。与对照小鼠相比,两种应激小鼠的NK、LAK和CTL活性以及NK受体均显著降低,但足部电击小鼠的降低幅度大于心理应激小鼠。仅在足部电击小鼠中颗粒酶A和穿孔素的mRNA转录本显著降低。另一方面,足部电击应激增加了颗粒酶B。上述发现表明,应激通过部分影响NK受体、颗粒酶和穿孔素诱导NK、LAK和CTL活性的抑制。

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