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Dexmedetomidine mitigates oxidative stress in H9C2 cardiac myoblasts under a high‑glucose environment via the PI3K/AKT signaling pathway

  • Authors:
    • Yan Qu
    • Wei Xiong
    • Rui Zhou
    • Ning Song
    • Jinqiao Qian

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  • Published online on: July 8, 2025     https://doi.org/10.3892/mmr.2025.13616
  • Article Number: 251

  • Copyright: © Qu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Dexmedetomidine (Dex) is a selective α2‑adrenergic receptor agonist used for its sedative effects in anesthesia and critical care. Although Dex exhibits cardioprotective effects, to the best of our knowledge, the mechanisms underlying these effects, particularly in a high‑glucose (HG) environment, remain unclear. Research into the role of Dex in alleviating oxidative stress injury in cardiac myoblasts through the PI3K/AKT signaling pathway may reveal novel cardioprotective mechanisms, enhance the understanding of cell survival and metabolic regulation, and offer potential clinical applications in cardiac surgery and critical care. The aim of the present study was to assess the protective effect and mechanism of Dex preconditioning (DP) against hydrogen peroxide (H2O2)‑induced H9C2 cardiac myoblast injury under HG conditions. H9C2 cardiac myoblasts were either untreated or pretreated with 10 nM Dex and the PI3K inhibitor LY294002 before exposure to H2O2 to induce oxidative cellular damage in the presence of HG culture medium. Cell viability assays were carried out, and apoptosis was evaluated using flow cytometry, TUNEL assays and western blotting. Additionally, the relative levels of oxidative stress indicators, including superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA), were determined. Exposure to H2O2 significantly decreased cell viability and increased apoptosis in H9C2 cardiac myoblasts cultured in HG conditions. Treatment with Dex significantly mitigated H2O2‑induced apoptosis, as evidenced by reduced expression of caspase‑3 and BAX, and increased levels of BCL‑2. In addition, oxidative stress was elevated in the HG + H2O2 group, as indicated by increased levels of the oxidative stress marker MDA, and reduced levels of the antioxidant enzymes SOD and CAT compared with those in the HG group. By contrast, DP in the DP + HG + H2O2 group reduced MDA levels, and increased SOD and CAT levels, indicating improved oxidative stress regulation. Treatment with the PI3K/AKT inhibitor LY294002 in the LY294002 + HG + DP + H2O2 group prevented these effects, further increasing MDA levels, and decreasing SOD and CAT levels compared with the DP + HG + H2O2 group, suggesting that the protective effects of Dex were abrogated by inhibition of the PI3K/AKT pathway. The present study revealed that Dex pretreatment attenuated H9C2 cardiac myoblast injury via the PI3K/AKT signaling pathway under HG conditions. Its protective effects may be achieved by reducing oxidative stress damage to cardiac myoblasts.
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September-2025
Volume 32 Issue 3

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

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  • Impact Factor: 3.5
  • Ranked Medicine Research and Experimental
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  • CiteScore: 8.5
  • CiteScore Rank: Q1: #78/441 Biochemistry, Genetics and Molecular Biology
  • Source Normalized Impact per Paper (SNIP): 0.772
  • SCImago Journal Rank (SJR): 0.841
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Spandidos Publications style
Qu Y, Xiong W, Zhou R, Song N and Qian J: Dexmedetomidine mitigates oxidative stress in H9C2 cardiac myoblasts under a high‑glucose environment via the PI3K/AKT signaling pathway. Mol Med Rep 32: 251, 2025.
APA
Qu, Y., Xiong, W., Zhou, R., Song, N., & Qian, J. (2025). Dexmedetomidine mitigates oxidative stress in H9C2 cardiac myoblasts under a high‑glucose environment via the PI3K/AKT signaling pathway. Molecular Medicine Reports, 32, 251. https://doi.org/10.3892/mmr.2025.13616
MLA
Qu, Y., Xiong, W., Zhou, R., Song, N., Qian, J."Dexmedetomidine mitigates oxidative stress in H9C2 cardiac myoblasts under a high‑glucose environment via the PI3K/AKT signaling pathway". Molecular Medicine Reports 32.3 (2025): 251.
Chicago
Qu, Y., Xiong, W., Zhou, R., Song, N., Qian, J."Dexmedetomidine mitigates oxidative stress in H9C2 cardiac myoblasts under a high‑glucose environment via the PI3K/AKT signaling pathway". Molecular Medicine Reports 32, no. 3 (2025): 251. https://doi.org/10.3892/mmr.2025.13616