HSP-17 protects H9c2 cells against oxidative stress injury and apoptosis by  activating  the  PI3K/Akt signalling pathway

Background : Oxidative stress and apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. HSP-17 is a peptide that is expressed at low levels in DOX-treated mouse heart tissue. It has high bioactivity and interspecies sequence consistency and is predicted to have a myocardial protective effect. Methods : First, we added 1 μM DOX to H9c2 cell culture medium and incubated the cells for 24 hours to construct a myocardial cytotoxicity model. Then, we detected the effect of HSP-17 on DOX-induced H9c2 cardiomyocyte injury by measuring cell viability and the level of lactate dehydrogenase (LDH). Furthermore, we used ROS and JC-1 kits to evaluate the effect of HSP-17 on oxidative stress injury in cardiomyocytes induced by DOX. Western blot and flow cytometry analyses were utilized to detect the level of apoptosis. Finally, we detected the protein expression levels of PI3K/Akt signalling pathway members by western blotting and demonstrated the cardioprotective mechanism of HSP-17. Results : We obtained evidence that the HSP-17 peptide can increase cell viability, reduce LDH levels, and reduce ROS and cardiomyocyte apoptosis. In addition, we provide evidence that HSP-17 upregulates the expression level of p-Akt in a DOX-induced cardiomyocyte injury model and that LY294002 (LY), a typical inhibitor of PI3K/Akt, eliminates the protective roles of HSP-17. Conclusions : In conclusion, we have elucidated, for the first time, that the HSP-17 peptide protects H9c2 cells against DOX-induced oxidative stress and apoptosis by activating the PI3K/Akt pathway, providing a new idea for the therapy of DOX-induced myocardial injury.