Zinc Attenuates the Cytotoxicity of Some Stimuli by Reducing Endoplasmic Reticulum Stress in Hepatocytes
Zinc Attenuates the Cytotoxicity of Some Stimuli by Reducing Endoplasmic Reticulum Stress in Hepatocytes
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DOI：
10.3390/ijms20092192
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发表时间：
2019-05
影响因子：
5.6
通讯作者：
Masashi Kusanaga;Shinji Oe;Noriyoshi Ogino;Sota Minami;Koichiro Miyagawa;Yuichi Honma;Masaru Harada
中科院分区：
文献类型：
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作者：
Masashi Kusanaga;Shinji Oe;Noriyoshi Ogino;Sota Minami;Koichiro Miyagawa;Yuichi Honma;Masaru Harada
锌是一种必需的微量元素，在细胞完整性和生物功能中起着关键作用。过量的铜诱导肝源性培养细胞的氧化应激和内质网（ER）应激。过量的铜还诱导自噬体-溶酶体融合步骤中的自噬通量受损，以及Mallory-Denk体（MDB）样包涵体的形成。锌通过维持内质网的稳态，改善了过量铜诱导的自噬通量和MDB样包涵体形成的损害。此外，锌还改善游离脂肪酸诱导的自噬通量的损害。这些结果表明，锌可能能够保护肝细胞免受各种ER应激相关的条件。
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.