PDF(Pubmed)
Abstract：
UNASSIGNED: Oxidative stress and cell apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. Heat shock protein-derived peptide (HSP-17) is a peptide which is low-expressed in DOX treated mouse heart tissue. It has high bioactivity and interspecies sequence consistency, and is predicted to have myocardial protective effect.
UNASSIGNED: Firstly, we added 1 µM DOX to H9c2 cell culture medium for 24 hours to construct the myocardial cytotoxicity model. Then we detected the effect of HSP-17 on DOX induced H9c2 cardiomyocyte injury by measuring cell viability and lactate dehydrogenase (LDH) level. In addition, reactive oxygen species (ROS) and tetraethylbenzimidazolylcarbocyanine iodide kits are used to evaluate the effect of the HSP-17 peptide on DOX-induced oxidative stress injury to cardiomyocytes, and the detection of apoptosis related proteins and flow cytometry were applied to detect the level of apoptosis. Furthermore, the protein expression levels [phosphorylated Akt (p-Akt) and phosphorylated PI3K (p-PI3K)] of the PI3K/Akt pathway were also detected by western blotting.
UNASSIGNED: We found that the HSP-17 peptide can increase cell viability, protect mitochondrial potential, reduce LDH levels, and reduce ROS and cardiomyocyte apoptosis. In addition, we also observed that HSP-17 upregulated the expression level of p-Akt, and LY294002, a typical inhibitor of PI3K/Akt, was found to eliminate the protective roles of HSP-17.
UNASSIGNED: In conclusion, this study demonstrated that the HSP-17 peptide protected H9c2 cells against oxidative stress and apoptosis via PI3K/Akt pathway activation, which provides a new idea for the treatment of DOX-induced myocardial injury.
UNASSIGNED: Firstly, we added 1 µM DOX to H9c2 cell culture medium for 24 hours to construct the myocardial cytotoxicity model. Then we detected the effect of HSP-17 on DOX induced H9c2 cardiomyocyte injury by measuring cell viability and lactate dehydrogenase (LDH) level. In addition, reactive oxygen species (ROS) and tetraethylbenzimidazolylcarbocyanine iodide kits are used to evaluate the effect of the HSP-17 peptide on DOX-induced oxidative stress injury to cardiomyocytes, and the detection of apoptosis related proteins and flow cytometry were applied to detect the level of apoptosis. Furthermore, the protein expression levels [phosphorylated Akt (p-Akt) and phosphorylated PI3K (p-PI3K)] of the PI3K/Akt pathway were also detected by western blotting.
UNASSIGNED: We found that the HSP-17 peptide can increase cell viability, protect mitochondrial potential, reduce LDH levels, and reduce ROS and cardiomyocyte apoptosis. In addition, we also observed that HSP-17 upregulated the expression level of p-Akt, and LY294002, a typical inhibitor of PI3K/Akt, was found to eliminate the protective roles of HSP-17.
UNASSIGNED: In conclusion, this study demonstrated that the HSP-17 peptide protected H9c2 cells against oxidative stress and apoptosis via PI3K/Akt pathway activation, which provides a new idea for the treatment of DOX-induced myocardial injury.
摘要：
未经证实：氧化应激和细胞凋亡在多柔比星（DOX）诱导的心肌损伤的发病机制中起关键作用。热休克蛋白衍生肽(HSP-17)是在DOX处理的小鼠心脏组织中低表达的肽。具有较高的生物活性和种间序列一致性,并预测具有心肌保护作用。
未经批准：首先，我们在H9c2细胞培养基中添加1µMDOX，持续24小时，以构建心肌细胞毒性模型。然后我们通过测量细胞活力和乳酸脱氢酶（LDH）水平来检测HSP-17对DOX诱导的H9c2心肌细胞损伤的影响。此外,活性氧（ROS）和四乙基苯并咪唑基碳花青碘化物试剂盒用于评估HSP-17肽对DOX诱导的心肌细胞氧化应激损伤的影响，细胞凋亡相关蛋白检测和流式细胞术检测细胞凋亡水平。此外，蛋白质印迹法检测PI3K/Akt途径的蛋白质表达水平[磷酸化Akt(p-Akt)和磷酸化PI3K(p-PI3K)]。
UNASSIGNED：我们发现HSP-17肽可以增加细胞活力，保护线粒体潜能，降低LDH水平，减少ROS和心肌细胞凋亡。此外,我们还观察到HSP-17上调p-Akt的表达水平，和LY294002，一种典型的PI3K/Akt抑制剂，发现消除了HSP-17的保护作用。
未经批准：总而言之，这项研究表明，HSP-17肽通过PI3K/Akt通路激活保护H9c2细胞免受氧化应激和凋亡，为治疗DOX诱导的心肌损伤提供了新的思路。
未经批准：首先，我们在H9c2细胞培养基中添加1µMDOX，持续24小时，以构建心肌细胞毒性模型。然后我们通过测量细胞活力和乳酸脱氢酶（LDH）水平来检测HSP-17对DOX诱导的H9c2心肌细胞损伤的影响。此外,活性氧（ROS）和四乙基苯并咪唑基碳花青碘化物试剂盒用于评估HSP-17肽对DOX诱导的心肌细胞氧化应激损伤的影响，细胞凋亡相关蛋白检测和流式细胞术检测细胞凋亡水平。此外，蛋白质印迹法检测PI3K/Akt途径的蛋白质表达水平[磷酸化Akt(p-Akt)和磷酸化PI3K(p-PI3K)]。
UNASSIGNED：我们发现HSP-17肽可以增加细胞活力，保护线粒体潜能，降低LDH水平，减少ROS和心肌细胞凋亡。此外,我们还观察到HSP-17上调p-Akt的表达水平，和LY294002，一种典型的PI3K/Akt抑制剂，发现消除了HSP-17的保护作用。
未经批准：总而言之，这项研究表明，HSP-17肽通过PI3K/Akt通路激活保护H9c2细胞免受氧化应激和凋亡，为治疗DOX诱导的心肌损伤提供了新的思路。
