Oxidative stress is a pivotal factor in the pathogenesis of various cardiovascular diseases. Rhodiola, a traditional Chinese medicine, is recognized for its potent antioxidant properties. Salidroside, a phenylpropanoid glycoside derived from Rhodiola rosea, has shown remarkable antioxidant capabilities. This study aimed to elucidate the potential protective mechanisms of Rhodiola and salidroside against H2O2‐induced cardiac apoptosis in H9c2 cardiomyoblast cells. H9c2 cells were exposed to H2O2 for 4 h, and subsequently treated with Rhodiola or salidroside for 24 h. Cell viability and apoptotic pathways were assessed. The involvement of insulin‐like growth factor 1 receptor (IGF1R) and the activation of extracellular regulated protein kinases 1/2 (ERK1/2) were investigated. H2O2 (100 μM) exposure significantly induced cardiac apoptosis in H9c2 cells. However, treatment with Rhodiola (12.5, 25, and 50 μg/mL) and salidroside (0.1, 1, and 10 nM) effectively attenuated H2O2‐induced cytotoxicity and apoptosis. This protective effect was associated with IGF1R‐activated phosphorylation of ERK1/2, leading to the inhibition of Fas‐dependent proteins, HIF‐1α, Bax, and Bak expression in H9c2 cells. The images from hematoxylin and eosin staining and immunofluorescence assays also revealed the protective effects of Rhodiola and salidroside in H9c2 cells against oxidative damage. Our findings suggest that Rhodiola and salidroside possess antioxidative properties that mitigate H2O2‐induced apoptosis in H9c2 cells. The protective mechanisms involve the activation of IGF1R and subsequent phosphorylation of ERK1/2. These results propose Rhodiola and salidroside as potential therapeutic agents for cardiomyocyte cytotoxicity and apoptosis induced by oxidative stress in heart diseases. Future studies may explore their clinical applications in cardiac health.

中文翻译：

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红景天和红景天苷通过 IGF1R 诱导的 ERK1/2 激活减弱氧化应激触发的 H9c2 成心肌细胞凋亡


氧化应激是各种心血管疾病发病机制的关键因素。红景天是一种传统中药，以其强大的抗氧化特性而闻名。红景天苷是一种源自红景天的苯丙烷苷，已显示出显着的抗氧化能力。本研究旨在阐明红景天和红景天苷对 H2O2 诱导的 H9c2 成心肌细胞心脏凋亡的潜在保护机制。将 H9c2 细胞暴露于 H 2 O 2 中 4 h，然后用红景天或红景天苷处理 24 h。评估细胞活力和凋亡途径。研究了胰岛素样生长因子 1 受体 （IGF1R） 的参与和细胞外调节蛋白激酶 1/2 （ERK1/2） 的激活。H 2 O 2 （100 μM） 暴露显着诱导 H9c2 细胞心脏凋亡。然而，用红景天（12.5、25 和 50 μg/mL）和红景天苷（0.1、1 和 10 nM）处理有效地减轻了 H 2 O 2 诱导的细胞毒性和细胞凋亡。这种保护作用与 IGF1R 激活的 ERK1/2 磷酸化有关，导致抑制 H9c2 细胞中 Fas 依赖性蛋白、HIF-1α、Bax 和 Bak 表达。来自苏木精和伊红染色以及免疫荧光测定的图像还揭示了红景天和红景天苷在 H9c2 细胞中对氧化损伤的保护作用。我们的研究结果表明，红景天和红景天苷具有抗氧化特性，可减轻 H2O2 诱导的 H9c2 细胞凋亡。保护机制涉及 IGF1R 的激活和随后的 ERK1/2 磷酸化。这些结果表明，红景天和红景天苷是心脏病中氧化应激诱导的心肌细胞细胞毒性和细胞凋亡的潜在治疗剂。 未来的研究可能会探索它们在心脏健康中的临床应用。