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Objective <p>The aim of this study was to investigate AMD1 cardiotoxicity function for Maduramicin (Mad).</p> Methods <p>SD rats were divided into control (Control) group and Mad treatment (3.5&#xa0;mg/kg) group (Mad). After treatment with Mad for seven days, the levels of LDH and CK-MB in serum were detected, H&amp;E staining and TUNEL staining were performed. In vitro, 1.0&#xa0;μm Mad was used for the subsequently experiment, observing cell apoptosis from Flow cytometry. Caspase-3 and AMD1 were detected in Western blotting. Flow cytometry and Western blotting were also performed after use of siRNA-AMD1-1. Then, analysis AMD1 potential function in cardiotoxicity from bioinformatics techniques including GO, KEGG, PPI, immune infiltration and molecular docking.</p> Result <p>Maduramicin has myocardial toxic effects in vivo and vitro, which with AMD1 raised. When AMD1 was knocked down, toxic effects of Mad were alleviated. Apoptosis, proliferation and inflammation were the major pathophysiological changes in myocardial apoptosis process with AMD1-knockdown. This process involved in <i>IL1A</i>,<i> IL1B</i>,<i> PTGS2</i>,<i> VEGFA</i>,<i> VEGFC and HBEFG</i>, as hub genes related AMD1 cardiotoxicity function for Maduramicin. AMD1 was knocked down, their microenvironment changes: Effector memory CD4 T cell and Natural killer cell were more infiltrated, and Mast cell were less infiltrated.</p> Conclusion <p>Mad exerted cardiotoxic effects by upregulating the AMD1 gene, which may be associated with cell apoptosis, proliferation and inflammatory response. AMD1 also had cardiotoxicity function, by the impact of both myocardial cells and the microenvironment they live.</p>

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AMD1, a cardiotoxicity target for Maduramicin

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年3月11日

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  • Zi-Feng Xie,
  • Han-Meng Liu,
  • Jia-Fan Zhao,
  • Yuan Gao,
  • Yuan-Long Zhao,
  • Jia-Yue Zheng,
  • Xiao-Wei Pei,
  • Ning Zhang,
  • Ge Tian

摘要

Objective

The aim of this study was to investigate AMD1 cardiotoxicity function for Maduramicin (Mad).

Methods

SD rats were divided into control (Control) group and Mad treatment (3.5 mg/kg) group (Mad). After treatment with Mad for seven days, the levels of LDH and CK-MB in serum were detected, H&E staining and TUNEL staining were performed. In vitro, 1.0 μm Mad was used for the subsequently experiment, observing cell apoptosis from Flow cytometry. Caspase-3 and AMD1 were detected in Western blotting. Flow cytometry and Western blotting were also performed after use of siRNA-AMD1-1. Then, analysis AMD1 potential function in cardiotoxicity from bioinformatics techniques including GO, KEGG, PPI, immune infiltration and molecular docking.

Result

Maduramicin has myocardial toxic effects in vivo and vitro, which with AMD1 raised. When AMD1 was knocked down, toxic effects of Mad were alleviated. Apoptosis, proliferation and inflammation were the major pathophysiological changes in myocardial apoptosis process with AMD1-knockdown. This process involved in IL1A, IL1B, PTGS2, VEGFA, VEGFC and HBEFG, as hub genes related AMD1 cardiotoxicity function for Maduramicin. AMD1 was knocked down, their microenvironment changes: Effector memory CD4 T cell and Natural killer cell were more infiltrated, and Mast cell were less infiltrated.

Conclusion

Mad exerted cardiotoxic effects by upregulating the AMD1 gene, which may be associated with cell apoptosis, proliferation and inflammatory response. AMD1 also had cardiotoxicity function, by the impact of both myocardial cells and the microenvironment they live.