Echinacoside reduced myocardial apoptosis and improved heart function in heart failure rats induced by isoproterenol via suppressing mitochondrial oxidative stress

[GW30-e0038]
Authors: Yajuan Ni, Deng Jie, Liu Xin, Li Qing, Ni Yajuan

Department of Cardiology, The Second Affiliated Hospital of Xi’an Jiaotong University

OBJECTIVES Apoptosis of myocardial cells has been shown to be a critical step provoking heart failure. Studies indicated that mitochondrial oxidative stress and excessive production of mitochondrial ROS in heart failure was tightly linked to activation of apoptosis. ECH was used as a traditional Chinese herbal medicine, it has been shown to possess powerful ability of anti-oxidant and anti-apoptosis properties in kinds of cells, but whether it affects myocardial apoptosis in the heart failure remain unknown. The present study investigated the effects of ECH on heart failure and myocardial apoptosis of rats induced by ISO in vivo and on mitochondrial oxidative stress of AC-16 cells induced by ISO and explored the underlying mechanisms in vitro.

METHODS Heart failure rats were induced by ISO, ECH was treated by intraperitoneal injection, echocardiography was performed to evaluate heart function, TUNEL was used to detect myocardial apoptosis in vivo. In vitro AC-16 cells were cultured, mitochondrial oxidative stress was induced by ISO, ECH was pre-treated. Apoptotic cells were detected by flow cytometry, the level of mitochondrial ROS were measured by luminol chemiluminescence, 8-OHdG was used to evaluate the oxidative damage of mitochondrial DNA, mitochondrial membrane potential was detected by JC-1, carbonylation of mitochondrial proteins were measured using Elisa, mitochondrial lipid peroxidation were measured using TBARS assay, intracellular ROS were measured with flow cytometry.

RESULTS The results demonstrated that ECH significantly improved the heart function and reduced myocardial apoptosis of heart failure rats induced by ISO in vivo, and inhibited oxidative damage of mitochondrial DNA, protected mitochondrial membrane potential, reduced intracellular ROS, prevented carbonylation of mitochondrial proteins and mitochondrial lipid peroxidation, suppressed production of mitochondrial ROS, and -subsequently inhibited intracellular ROS of AC-16 cells induced by ISO in vitro.

CONCLUSIONS We concluded that ECH significantly inhibited myocardial apoptosis and improved heart function of heart failure rats induced by ISO via suppressing mitochondrial oxidative stress. It was suggested that ECH was a potential drug treatment for heart failure.