Why the study?
Although dexmedetomidine exhibits cardioprotective effects, the mechanisms underlying these effects, particularly in a high-glucose environment, remained unclear.
Does dexmedetomidine prevent oxidative stress and apoptosis in H9C2 cardiac myoblasts under high-glucose conditions?
Does dexmedetomidine prevent oxidative stress and apoptosis in H9C2 cardiac myoblasts under high-glucose conditions?
Dexmedetomidine protects cardiac myoblasts from oxidative stress and apoptosis in a high-glucose environment via the PI3K/AKT signaling pathway, suggesting potential utility in diabetic cardiomyopathy.
Hypothesis-generating for dexmedetomidine in diabetic cardiomyopathy; does not support practice change without clinical trials.
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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Qü et al. (2025) studied this question.
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