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

作者：Yan Qü, Wei Xiong, Rui Zhou, Ning Song, Jinqiao Qian · 发表于：Molecular Medicine Reports · 年份：2025 · DOI：10.3892/mmr.2025.13616 · 被引用次数：4 · 研究领域：Cardiac Ischemia and Reperfusion、Nitric Oxide and Endothelin Effects、Cardiovascular Function and Risk Factors

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 (H 2 O 2 )‑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 H 2 O 2 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 H 2 O 2 significantly decreased cell viability and increased apoptosis in H9C2 cardiac myoblasts cultured in HG conditions. Treatment with Dex s...