Open Access

H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy

  • Authors:
    • Guodong Cao
    • Youcheng Zeng
    • Yuhan Zhao
    • Liang Lin
    • Xiqing Luo
    • Lichun Guo
    • Yixin Zhang
    • Qinghong Cheng
  • View Affiliations

  • Published online on: September 12, 2022     https://doi.org/10.3892/mmr.2022.12851
  • Article Number: 335
  • Copyright: © Cao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Ferroptosis is a non‑apoptotic form of cell death mediated by reactive oxygen species (ROS). Iron metabolism disorders play a key role in sepsis‑induced cardiomyopathy (SIC). While hydrogen sulfide (H2S) inhibits SIC, it is unknown if it does so by controlling ferroptosis. The present study evaluated whether sodium hydrosulfide (NaHS), an H2S donor, alleviates SIC by decreasing ferroptosis. Lipopolysaccharide (LPS) was employed to induce an in vitro model of septic myocardial injury in rat H9c2 cardiomyocytes. The myocardial injury model of septic rats was established by cecal ligation and puncture (CLP). Cardiomyocyte injury was evaluated using Cell Counting Kit‑8 and myocardial enzyme assay and hematoxylin and eosin (H&E) staining. The cardiac function of rats was assessed using echocardiography and changes in myocardial fibers and mitochondria were evaluated using H&E staining and transmission electron microscopy, respectively. Fe2+, glutathione and malondialdehyde levels in cardiomyocytes were detected using assay kits, ROS and mitochondrial membrane potential changes were detected using fluorescent probes and ferroptosis and Beclin 1 (BECN1) signaling pathway‑associated protein expression levels were semi‑quantified using western blotting. NaHS decreased ferroptosis of H9c2 cells induced by LPS and decreased injury of myocardial cells by improving iron metabolism disorder and oxidative stress levels. Furthermore, in vivo results demonstrated that NaHS attenuated CLP‑induced septic myocardial ferroptosis and significantly improved cardiac dysfunction in septic rats compared with the CLP group. NaHS was demonstrated to attenuate sepsis‑induced myocardial cell and tissue injury by significantly inhibiting the phosphorylation of BECN1 and significantly increasing expression levels of the ferroptosis regulatory proteins solute carrier family 7 member 11 and glutathione peroxidase 4. The results of the present study suggested that by regulating the BECN1 signaling pathway, NaHS may decrease the incidence of myocardial ferroptosis, thereby improving SIC.
View Figures
View References

Related Articles

Journal Cover

November-2022
Volume 26 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Cao G, Zeng Y, Zhao Y, Lin L, Luo X, Guo L, Zhang Y and Cheng Q: H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy. Mol Med Rep 26: 335, 2022
APA
Cao, G., Zeng, Y., Zhao, Y., Lin, L., Luo, X., Guo, L. ... Cheng, Q. (2022). H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy. Molecular Medicine Reports, 26, 335. https://doi.org/10.3892/mmr.2022.12851
MLA
Cao, G., Zeng, Y., Zhao, Y., Lin, L., Luo, X., Guo, L., Zhang, Y., Cheng, Q."H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy". Molecular Medicine Reports 26.5 (2022): 335.
Chicago
Cao, G., Zeng, Y., Zhao, Y., Lin, L., Luo, X., Guo, L., Zhang, Y., Cheng, Q."H2S regulation of ferroptosis attenuates sepsis‑induced cardiomyopathy". Molecular Medicine Reports 26, no. 5 (2022): 335. https://doi.org/10.3892/mmr.2022.12851