Rapid restoration of perfusion in ischemic myocardium is the most direct and effective treatment for coronary heart disease but may cause myocardial ischemia/reperfusion injury (MIRI). Cinnamaldehyde (CA, C9H8O), a key component in the well‐known Chinese medicine cinnamomum cassia, has cardioprotective effects against MIRI. This study aimed to observe the therapeutic effect of CA on MIRI and to elucidate its potential mechanism. H9C2 rat cardiomyocytes were pretreated with CA solution at 0, 10, and 100 μM, respectively and subjected to oxygen‐glucose deprivation/reoxygenation (OGD/R). Then the cell viability, the NF‐κB and caspase3 gene levels, the reduced glutathione (GSH)/oxidized glutathione (GSSG) ratio, superoxide dismutase (SOD) level, reactive oxygen species (ROS) generation, 4‐hydroxynonenal (4‐HNE), and malondialdehyde (MDA) were detected. The severity of DNA damage was assessed by tail moment (TM) values using alkaline comet assay. Besides, the DNA damage‐related proteins and the key proteins of the Nrf2 pathway were detected by western blot. CA treatment increased the cell viability, GHS/GSSG ratio, SOD level, PARP1, Nrf2, PPAR‐γ, and HO‐1 protein levels of H9C2 cardiomyocytes, while reducing NF‐κB, caspase3, ROS level, 4‐HNE and MDA content, γ‐H2AX protein level, and TM values. Inhibition of the Nrf2 pathway reversed the effect of CA on cell viability and apoptosis of OGD/R induced H9C2 cardiomyocytes. Besides, 100 μM CA was more effective than 10 μM CA. In the OGD/R‐induced H9C2 cardiomyocyte model, CA can protect cardiomyocytes from MIRI by attenuating lipid peroxidation and repairing DNA damage. The mechanism may be related to the activation of the Nrf2 pathway.

中文翻译：

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肉桂醛通过激活 Nrf2 通路保护心肌细胞免受氧糖剥夺/复氧诱导的脂质过氧化和 DNA 损伤

快速恢复缺血心肌的灌注是治疗冠心病最直接有效的方法，但可能会引起心肌缺血/再灌注损伤（MIRI）。肉桂醛（CA，C9H8O）是著名中药肉桂的关键成分，对 MIRI 具有心脏保护作用。本研究旨在观察CA对MIRI的治疗作用并阐明其潜在机制。H9C2大鼠心肌细胞分别用0、10和100μM的CA溶液预处理，并进行氧糖剥夺/复氧（OGD/R）。然后是细胞活力、NF-κB 和 caspase3 基因水平、还原型谷胱甘肽 (GSH)/氧化型谷胱甘肽 (GSSG) 比率、超氧化物歧化酶 (SOD) 水平、活性氧 (ROS) 生成、4-羟基壬烯醛 (4-HNE) ）和丙二醛（MDA）被检测到。使用碱性彗星测定通过尾矩 (TM) 值评估 DNA 损伤的严重程度。此外，通过蛋白质印迹法检测DNA损伤相关蛋白和Nrf2通路的关键蛋白。CA处理增加了H9C2心肌细胞的细胞活力、GHS/GSSG比值、SOD水平、PARP1、Nrf2、PPAR-γ和HO-1蛋白水平，同时降低了NF-κB、caspase3、ROS水平、4-HNE和MDA含量、γ-H2AX 蛋白水平和 TM 值。Nrf2 通路的抑制逆转了 CA 对 OGD/R 诱导的 H9C2 心肌细胞的细胞活力和凋亡的影响。此外，100 μM C​​A 比 10 μM C​​A 更有效。在 OGD/R 诱导的 H9C2 心肌细胞模型中，CA 可以通过减弱脂质过氧化和修复 DNA 损伤来保护心肌细胞免受 MIRI 的影响。其机制可能与Nrf2通路的激活有关。