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Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress-induced apoptosis in H9c2 cardiomyocytes 期刊论文

编号：

ec507eba-60de-4024-98b7-efa8d284149a
作者：

Sun, MengYao(孙孟尧)#^[1]Ma, DaShi(马大实)^[1]Zhao, Song(赵松)^[2]Wang, Lei(王磊)^[1]Ma, ChunYe(马春野)^[1]Bai, Yang(白杨)*^[1]
语种：

英文
期刊：

MOLECULAR MEDICINE REPORTS ISSN：1791-2997 2018 年 18 卷 4 期 (3760 - 3768) ; OCT
收录：
关键词：

salidroside myocardial ischemia reperfusion injury endoplasmic reticulum stress apoptosis cardioprotection
摘要：

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.
推荐引用方式
GB/T 7714：

Sun Meng-Yao,Ma Da-Shi,Zhao Song, et al. Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress-induced apoptosis in H9c2 cardiomyocytes [J].MOLECULAR MEDICINE REPORTS,2018,18(4):3760-3768.
APA：

Sun Meng-Yao,Ma Da-Shi,Zhao Song,Wang Lei,&Bai Yang.(2018).Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress-induced apoptosis in H9c2 cardiomyocytes .MOLECULAR MEDICINE REPORTS,18(4):3760-3768.
MLA：

Sun Meng-Yao, et al. "Salidroside mitigates hypoxia/reoxygenation injury by alleviating endoplasmic reticulum stress-induced apoptosis in H9c2 cardiomyocytes" .MOLECULAR MEDICINE REPORTS 18,4(2018):3760-3768.
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