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心理应激诱导大鼠肝脏锌蓄积以及锌转运体14(ZIP14)和金属硫蛋白上调。

Psychological stress induced zinc accumulation and up-regulation of ZIP14 and metallothionein in rat liver.

作者信息

Tian Xue, Zheng Yuanyuan, Li Yingjie, Shen Zhilei, Tao Liping, Dou Xiao, Qian Jianxin, Shen Hui

机构信息

Department of Naval Hygiene, Second Military Medical University, 800 Xiangyin Road, Shanghai 200433, PR China.

出版信息

BMC Gastroenterol. 2014 Feb 18;14:32. doi: 10.1186/1471-230X-14-32.

Abstract

BACKGROUND

Zinc is necessary for normal liver function; and vice versa, the liver plays a central role in zinc homeostasis. The aim of present study is to assess the effects of repeated psychological stress (PS) on the zinc metabolism and related mechanism involved in zinc homeostasis in rat liver.

METHODS

In present study, we used communication box to create PS model and investigated the serum corticosterone (CORT), zinc level in serum and liver, liver metallothionein (MT) content and ZRT/IRT-like Protein 14 (ZIP14) mRNA expression.

RESULTS

The results showed that the serum CORT level increased and serum zinc level decreased significantly after 7 d and 14 d PS treatment. Meanwhile, zinc and MT contents in liver were elevated after 14 d PS exposure, while those in 7 d PS exposure group did not change. ZIP14 mRNA was expressed markedly at 7 d after the onset of PS, while Zip14 mRNA expression in the liver after 14 d PS exposure reached normal level compared with control group.

CONCLUSIONS

The results suggest that PS exposure could induce hypozincemia, which might be related to liver zinc accumulation because of high level of MT through glucocorticoid-mediated MT synthesis and ZIP14 expression induced by interleukin-6.

摘要

背景

锌对于正常肝功能是必需的;反之,肝脏在锌稳态中起核心作用。本研究的目的是评估反复心理应激(PS)对大鼠肝脏锌代谢及锌稳态相关机制的影响。

方法

在本研究中,我们使用交流箱建立PS模型,并检测血清皮质酮(CORT)、血清和肝脏中的锌水平、肝脏金属硫蛋白(MT)含量以及锌转运体/铁调节转运蛋白样蛋白14(ZIP14)mRNA表达。

结果

结果显示,PS处理7天和14天后,血清CORT水平升高,血清锌水平显著降低。同时,PS暴露14天后肝脏中的锌和MT含量升高,而7天PS暴露组则无变化。PS开始后7天,ZIP14 mRNA显著表达,而PS暴露14天后肝脏中Zip14 mRNA表达与对照组相比恢复到正常水平。

结论

结果表明,PS暴露可导致低锌血症,这可能与肝脏锌蓄积有关,其机制可能是通过糖皮质激素介导MT合成以及白细胞介素-6诱导ZIP14表达,导致MT水平升高。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5f8c/3931483/865854c36dfc/1471-230X-14-32-1.jpg

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