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Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway

  • Authors:
    • Wenmao Zhang
    • Ziling Liao
    • Chengfeng Xu
    • Xinping Lin
  • View Affiliations / Copyright

    Affiliations: Department of Scientific Research, Yueyang Maternal and Child Health‑Care Hospital, Yueyang, Hunan 414000, P.R. China, Department of Research and Development, Beijing Zhongwei Research Center of Biological and Translational Medicine, Beijing 100000, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 180
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    Published online on: October 2, 2024
       https://doi.org/10.3892/br.2024.1868
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Abstract

Myocardial infarction is characterized by oxygen deficiency caused by arterial flow restriction. Salidroside (SAL) protects against myocardial damage via antioxidant production and inhibition of apoptosis. The present study aimed to investigate potential rescue mechanism of SAL on hypoxic cardiomyocytes. H9C2 cardiomyocytes were divided into normoxia, hypoxia and hypoxia + SAL groups. The inhibitory rate of hypoxia and the optimal concentration and rescue effect of SAL were determined using Cell Counting Kit‑8 assay and flow cytometry. Ca2+ concentration following hypoxia treatment and SAL intervention were detected by Fluo‑4/acetoxymethyl. Tandem mass tag (TMT) proteomics was used to analyze the differential expression of hypoxia‑associated proteins among the three groups. SAL exerted a protective effect on hypoxia‑injured cardiomyocytes by enhancing aerobic metabolism during hypoxia and rescuing cardiomyocytes from hypoxic damage. SAL promoted cell proliferation, decreased apoptosis and increased Ca2+ levels in cell membranes of hypoxic cardiomyocytes. TMT proteomics results showed that the expression levels of intracellular hypoxia inducible factor‑1 (HIF)‑1α and Egl‑9 family HIF 1 (EGLN1) in H9C2 cells were elevated under hypoxic conditions. However, SAL significantly decreased expression levels of HIF‑1α and EGLN1. SAL inhibited mitochondrial calcium overload in hypoxic cardiomyocytes and attenuated expression of hypoxia‑associated factors. SAL exerted its rescue effect on hypoxic cardiomyocytes through the EGLN1/HIF‑1α pathway, thereby suppressing cardiomyocyte apoptosis, improving mitochondrial energy metabolism efficiency and rescuing cardiomyocytes from hypoxic injury.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang W, Liao Z, Xu C and Lin X: Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway. Biomed Rep 21: 180, 2024.
APA
Zhang, W., Liao, Z., Xu, C., & Lin, X. (2024). Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway. Biomedical Reports, 21, 180. https://doi.org/10.3892/br.2024.1868
MLA
Zhang, W., Liao, Z., Xu, C., Lin, X."Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway". Biomedical Reports 21.6 (2024): 180.
Chicago
Zhang, W., Liao, Z., Xu, C., Lin, X."Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway". Biomedical Reports 21, no. 6 (2024): 180. https://doi.org/10.3892/br.2024.1868
Copy and paste a formatted citation
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Spandidos Publications style
Zhang W, Liao Z, Xu C and Lin X: Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway. Biomed Rep 21: 180, 2024.
APA
Zhang, W., Liao, Z., Xu, C., & Lin, X. (2024). Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway. Biomedical Reports, 21, 180. https://doi.org/10.3892/br.2024.1868
MLA
Zhang, W., Liao, Z., Xu, C., Lin, X."Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway". Biomedical Reports 21.6 (2024): 180.
Chicago
Zhang, W., Liao, Z., Xu, C., Lin, X."Salidroside rescues hypoxic cardiomyocytes by regulating the EGLN1/HIF‑1α pathway". Biomedical Reports 21, no. 6 (2024): 180. https://doi.org/10.3892/br.2024.1868
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