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白细胞介素-1诱导血清锌和肝脏金属硫蛋白水平变化的糖皮质激素非依赖性介导作用。

Glucocorticoid independent mediation of interleukin-1 induced changes in serum zinc and liver metallothionein levels.

作者信息

DiSilvestro R A, Cousins R J

出版信息

Life Sci. 1984 Nov 19;35(21):2113-8. doi: 10.1016/0024-3205(84)90510-1.

Abstract

Interleukin-1 (IL-1) causes changes in zinc metabolism which have been attributed to mediation, at least in part, by glucocorticoids. However, IL-1 was found to actually lower serum corticosterone levels in rats. In addition, adrenalectomy only partially inhibited the ability of IL-1 to depress serum zinc levels and increase the amount of zinc associated with hepatic metallothionein. Furthermore, IL-1 increased total liver metallothionein protein to similar levels in both adrenalectomized and normal rats. Administering the synthetic glucocorticoid dexamethasone with IL-1 to adrenalectomized rats produced additive, but not synergistic effects on serum zinc and metallothionein concentrations. Studies with actinomycin D suggested that IL-1 induction of metallothionein might involve glucagon.

摘要

白细胞介素-1(IL-1)会引起锌代谢的变化,这种变化至少部分归因于糖皮质激素的介导作用。然而,研究发现IL-1实际上会降低大鼠血清皮质酮水平。此外,肾上腺切除术仅部分抑制了IL-1降低血清锌水平以及增加与肝脏金属硫蛋白相关的锌含量的能力。此外,IL-1使肾上腺切除大鼠和正常大鼠的肝脏金属硫蛋白总蛋白增加到相似水平。对肾上腺切除大鼠同时给予合成糖皮质激素地塞米松和IL-1,对血清锌和金属硫蛋白浓度产生相加而非协同作用。用放线菌素D进行的研究表明,IL-1对金属硫蛋白的诱导可能涉及胰高血糖素。

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