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Funding Acknowledgements Type of funding sources: Other. Main funding source(s): Shaanxi Provincial Key Research and Development Projects (2019SF-218) Background Endoplasmic reticulum (ER) stress played an essential role in the development and progression of HF due to it could induce cardiomyocyte apoptosis, ATF6/CHOP was regulated by NADPH and ROS and was the crucial pathway to link ER stress and apoptosis in HF. Our previous study indicated that ECH reversed cardiac remodeling and improves heart function, but the underlying mechanisms are still unclear. Objectives To investigate the effect of ECH on cardiomyocyte apoptosis and endoplasmic reticulum stress and the underlying mechanisms. Methods In vitro, we cultured AC-16 cells and induced cell damage and ER stress by ISO, treated by ECH, the cell apoptosis and biomarkers of ER stress (GRP78, ATF6α, IRE1α, PERK) were detected. In vivo, we induced HF rat model by ISO and treated by ECH, indexes of heart function, cardiomyocyte apoptosis, biomarkers of ER stress and NADPH/ROS/ATF6/CHOP pathway were measured. Results In vitro, we confirmed that ECH inhibited ER stress and apoptosis. In vivo, we demonstrated that ECH inhibited cardiomyocyte apoptosis and improved heart function, it significantly decreased GRP78, ATF6α, IRE1α, PERK, and down-regulated NADPH/ROS/ATF6/CHOP pathway. Conclusions ECH inhibited cardiomyocyte apoptosis and improved heart function via suppressing NADPH/ROS/ATF6/CHOP pathway associated ER stress.

european heart journal

Echinacoside inhibited cardiomyocyte apoptosis and improved heart function in heart failure rats induced by isoproterenol via suppressing nadph/ros/atf6/chop associated endoplasmic reticulum stress