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硒蛋白 M 敲除在褪黑素拮抗镍诱导的小鼠心脏细胞凋亡和内质网应激中的作用

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  • Additional Information
    • Publication Information:
      Zhejiang University Press, 2023.
    • Publication Date:
      2023
    • Abstract:
      The aim of this study was to investigate the role of selenoprotein M (SelM) in endoplasmic reticulum stress and apoptosis in nickel-exposed mouse hearts and to explore the detoxifying effects of melatonin. At 21 d after intraperitoneal injection of nickel chloride (NiCl(2)) and/or melatonin into male wild-type (WT) and SelM knockout (KO) C57BL/6J mice, NiCl(2) was found to induce changes in the microstructure and ultrastructure of the hearts of both WT and SelM KO mice, which were caused by oxidative stress, endoplasmic reticulum stress, and apoptosis, as evidenced by decreases in malondialdehyde (MDA) content and total antioxidant capacity (T-AOC) activity. Changes in the messenger RNA (mRNA) and protein expression of genes related to endoplasmic reticulum stress (activating transcription factor 4 (ATF4), inositol-requiring protein 1 (IRE1), c-Jun N-terminal kinase (JNK), and C/EBP homologous protein (CHOP)) and apoptosis (B-cell lymphoma-2 (Bcl-2), Bcl-2-associated X protein (Bax), Caspase-3, Caspase-9, and Caspase-12) were also observed. Notably, the observed damage was worse in SelM KO mice. Furthermore, melatonin alleviated the heart injury caused by NiCl(2) in WT mice but could not exert a good protective effect in the heart of SelM KO mice. Overall, the findings suggested that the antioxidant capacity of SelM, as well as its modulation of endoplasmic reticulum stress and apoptosis, plays important roles in nickel-induced heart injury.
    • ISSN:
      1862-1783
      1673-1581
    • Rights:
      OPEN
    • Accession Number:
      edsair.doi.dedup.....b727785f65eacd2831df5d7edc7a6fd9