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Immunosuppression induced by central action of morphine is not blocked by mifepristone (RU 486).

机译:通过吗啡的中枢作用诱导的免疫抑制不受米非司酮(RU 486)的阻断。

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Morphine causes immunosuppression by binding to opioid receptors on immune cells, or indirectly by acting on receptors in the brain. However, morphine exact mechanism of action has not been elucidated. In the present study, we investigated the role of glucocorticoids in morphine-mediated immunosuppression after acute action in the rat mesencephalon periaqueductal gray (PAG). Natural killer (NK) cell activity and T cell proliferation were used to evaluate potential indirect mechanisms of morphine action. Microinjection of morphine in the ventral-caudal aspect of the PAG significantly (p < 0.01) suppressed splenic NK cell cytotoxic activity (32% reduction), and antiTCR-, IL-2-, antiTCR + IL-2, and Con A-induced thymic (30% to 50% reduction) and splenic (35% to 70% reduction) lymphocyte proliferation compared with PAG-injected saline control animals. The glucocorticoid receptor antagonist mifepristone (RU 486) did not block the immunosuppressive effects of morphine, suggesting that such effects are independent of activation of the hypothalamic-pituitary-adrenal axis.
机译:吗啡通过与免疫细胞上的阿片受体结合或间接作用于大脑中的受体而引起免疫抑制。但是,吗啡的确切作用机理尚未阐明。在本研究中,我们调查了大鼠中脑导水管周围灰色(PAG)急性作用后糖皮质激素在吗啡介导的免疫抑制中的作用。自然杀伤(NK)细胞活性和T细胞增殖被用来评估吗啡作用的潜在间接机制。在PAG腹侧尾部微量注射吗啡显着(p <0.01)抑制了脾NK细胞的细胞毒活性(降低了32%),并且抗TCR-,IL-2-,抗TCR + IL-2和Con A诱导与注射PAG的盐水对照组动物相比,胸腺(减少了30%至50%)和脾脏(减少了35%至70%)淋巴细胞增殖。糖皮质激素受体拮抗剂米非司酮(RU 486)不能阻断吗啡的免疫抑制作用,表明这种作用与下丘脑-垂体-肾上腺轴的激活无关。

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