01357bc5-1a81-415f-8158-fc5654cda4f8
Effect of HSP-17 peptide on gene expression of doxorubicin-treated H9c2 cells.
Oxidative stress and cell apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. HSP-17 is a peptide that is lowly expressed in heart tissue from DOX-treated mice. It has a high bioactivity and interspecies sequence consistency, and is predicted to have myocardial protective effects. We have proved that HSP-17 peptide can increase cell viability, protect mitochondrial potential, reduce LDH levels, and reduce ROS and cardiomyocyte apoptosis. To investigate the  mechanism underlying cardioprotective role of  HSP-17, H9c2 cells were pretreated with 10 µM HSP-17 or scramble peptide for 2 hrs and then insuled by 1 µM DOX for 24 hrs.Total RNA was harvested, and then subjected to quality control and purification. cDNA libraries were created and sequenced on an Illumina HiSeq System.
Oxidative stress and cell apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. HSP-17 is a peptide that is lowly expressed in heart tissue from DOX-treated mice. It has a high bioactivity and interspecies sequence consistency, and is predicted to have myocardial protective effects. We have proved that HSP-17 peptide can increase cell viability, protect mitochondrial potential, reduce LDH levels, and reduce ROS and cardiomyocyte apoptosis. To investigate the  mechanism underlying cardioprotective role of  HSP-17, H9c2 cells were pretreated with 10 µM HSP-17 or scramble peptide for 2 hrs and then insuled by 1 µM DOX for 24 hrs.Total RNA was harvested, and then subjected to quality control and purification. cDNA libraries were created and sequenced on an Illumina HiSeq System.