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锌通过减少肝细胞内质网应激减轻某些刺激物的细胞毒性。

Zinc Attenuates the Cytotoxicity of Some Stimuli by Reducing Endoplasmic Reticulum Stress in Hepatocytes.

机构信息

Third Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.

出版信息

Int J Mol Sci. 2019 May 3;20(9):2192. doi: 10.3390/ijms20092192.

DOI:10.3390/ijms20092192
PMID:31058829
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6540033/
Abstract

Zinc is an essential trace element and plays critical roles in cellular integrity and biological functions. Excess copper induced both oxidative stress and endoplasmic reticulum (ER) stress in liver-derived cultured cells. Excess copper also induced impairment of autophagic flux at the step of autophagosome-lysosome fusion, as well as Mallory-Denk body (MDB)-like inclusion body formation. Zinc ameliorated excess copper-induced impairment of autophagic flux and MDB-like inclusion body formation via the maintenance of ER homeostasis. Furthermore, zinc also ameliorated free fatty acid-induced impairment of autophagic flux. These results indicate that zinc may be able to protect hepatocytes from various ER stress-related conditions.

摘要

锌是一种必需的微量元素,在细胞完整性和生物功能中发挥着关键作用。过量的铜会在肝源性培养细胞中引起氧化应激和内质网(ER)应激。过量的铜还会导致自噬小体-溶酶体融合步骤中的自噬流受损,以及形成 Mallory-Denk 体(MDB)样包涵体。锌通过维持内质网的稳态来改善过量铜引起的自噬流和 MDB 样包涵体形成的损伤。此外,锌还可以改善游离脂肪酸引起的自噬流损伤。这些结果表明,锌可能能够保护肝细胞免受各种与内质网应激相关的情况的影响。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69d6/6540033/d8bb15a3d314/ijms-20-02192-g005.jpg
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本文引用的文献

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Recent Advances in the Role of SLC39A/ZIP Zinc Transporters In Vivo.SLC39A/ZIP 锌转运体在体内作用的最新进展。
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Lipid-Induced Endoplasmic Reticulum Stress Impairs Selective Autophagy at the Step of Autophagosome-Lysosome Fusion in Hepatocytes.
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