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首页> 外文期刊>Molecular medicine reports >Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress-induced apoptosis in H9c2 cardiomyocytes
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Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress-induced apoptosis in H9c2 cardiomyocytes

机译：Salidroside通过减轻H9C2心肌细胞中的内质网胁迫诱导的细胞凋亡来减轻缺氧/雷诺酸损伤

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Endoplasmic reticulum (ER) stress-induced apoptosis serves a crucial role in the development of myocardial ischemia/reperfusion (I/R) injury. Salidroside is a phenylpropanoid glycoside isolated from Rhodiola rosea L., which is a plant often used in traditional Chinese medicine. It possesses multiple pharmacological actions and protects against myocardial I/R injury in vitro and in vivo. However, it is not yet clear whether ER stress or ER stress-induced apoptosis contributes to the cardioprotective effects of salidroside against myocardial I/R injury. Hence, hypoxia/reoxygenation (H/R)-treated H9c2 cardiomyocytes were used in the current study to mimic myocardium I/R injury in vivo. It was hypothesized that salidroside alleviates ER stress and ER stress-induced apoptosis, thereby reducing H/R injury in H9c2 cells. The results demonstrated that salidroside attenuated H/R-induced H9c2 cardiomyocyte injury, as cell viability was increased, lactate dehydrogenase release was decreased, morphological changes in apoptotic cells were ameliorated and the apoptosis ratio was reduced compared with the H/R group. ER stress was reversed, indicated by the downregulation of glucose regulated protein 78 and C/EBP homologous protein following pretreatment with salidroside. In addition, salidroside attenuated ER stress-induced apoptosis, as the expression of cleaved caspase-12 and pro-apoptotic protein Bcl-2 associated X protein and activity of caspase-3 was decreased, while the expression of anti-apoptotic protein Bcl-2 was increased following pretreatment with salidroside. Furthermore, the results indicated that salidroside decreases the activation of the ER stress-associated signaling pathway, as the expression of phosphorylated protein kinase RNA (PKR)-like ER kinase (p-PERK) and phosphorylated inositol-requiring enzyme-1 (p-IRE1) proteins were decreased following pretreatment with salidroside. These results demonstrate that salidroside protects against H/R injury via regulation of the PERK and IRE1 pathways, resulting in alleviation of ER stress or ER stress-induced apoptosis in H9c2 cardiomyocytes.
机译：内质网（ER）应激诱导的细胞凋亡在心肌缺血/再灌注（I / R）损伤方面发挥至关重要作用。 Salidroside是一种从Rhodiola Rosea L中分离的苯丙二醇糖苷，它是通常用于中药中的植物。它具有多种药理作用，并在体外和体内免受心肌I / R损伤。然而，尚不清楚ER应激或ER应激诱导的细胞凋亡是否有助于Salidroside对心肌I / R损伤的心脏保护作用。因此，在目前的研究中使用缺氧/再氧化（H / R）-Treated H9C2心肌细胞以模仿体内的心肌I / R损伤。假设Salidroside减轻了ER应激和ER应激诱导的细胞凋亡，从而降低了H9C2细胞中的H / R损伤。结果表明，随着细胞活力的增加，Salidroside衰减H / R诱导的H9C2心肌细胞损伤，降低了乳酸脱氢酶释放，改善了凋亡细胞的形态变化，与H / R组相比，凋亡率降低。反转ER应激，通过葡萄糖调节蛋白质78和C / EBP同源蛋白质的预处理后的葡萄糖调节蛋白质78和C / EBP同源蛋白表明。此外，Salidroside衰减ER应激诱导的细胞凋亡，因为切割的caspase-12和促凋亡蛋白Bcl-2相关X蛋白和Caspase-3的活性的表达减少，而抗凋亡蛋白Bcl-2的表达表达用Salidroside预处理后增加。此外，结果表明，Salidroside降低了ER应激相关信号传导途径的激活，作为磷酸化蛋白激酶RNA（PKR） - 样ER激酶（P-PERK）和磷酸化的肌醇需要酶-1的表达（P-在用Salidroside预处理后，IS1）蛋白质降低。这些结果表明，Salidroside通过调节Perk和IS1途径来保护H / R损伤，导致缓解H9C2心肌细胞中的ER应激或ER应激诱导的细胞凋亡。

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