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Abstract
Endoplasmic reticulum stress (ERS) is one of the mechanisms of apoptotic cell death. Inhibiting the apoptosis induced by ERS may be a novel therapeutic target in cardiovascular diseases. Icariin, a flavonoid isolated from Epimedium brevicornum Maxim, has been demonstrated to have cardiovascular protective effects, but its effects on ERS are unknown. In the present study, we focused on icariin and investigated whether it might protect the cardiac cell from apoptosis via inhibition of ERS. In H9c2 rat cardiomyoblast cells, pretreatment of icariin significantly inhibited cell apoptosis by tunicamycin, an ERS inducer. Icariin also decreased generation of reactive oxygen species (ROS), loss of mitochondrial membrane potential and activation of caspase-3. Moreover, icariin inhibited upregulation of endoplasmic reticulum markers, GRP78, GRP94 and CHOP, elicited by tunicamycin. These results indicated that icariin could protect H9c2 cardiomyoblast cells from ERS-mitochondrial apoptosis in vitro, the mechanisms may be associated with its inhibiting of GRP78, GRP94 and CHOP and decreasing ROS generation directly. It may be a potential agent for treating cardiovascular disease.
Highlights
Endoplasmic reticulum stress (ERS) is involved in cardiovascular pathological processes, such as atherosclerosis, ischemic heart disease, cardiomyopathy and heart failure
The results showed that icariin could protect H9c2 cells from tunicamycin-induced cell death in a concentration-dependent manner
We found that icariin inhibited the effects of tunicamycin to increase the cell viability and decrease apoptosis in H9c2 cells
Summary
Endoplasmic reticulum stress (ERS) is involved in cardiovascular pathological processes, such as atherosclerosis, ischemic heart disease, cardiomyopathy and heart failure. In pressure overloaded heart failure, the ERS markers, glucose-regulated protein 78 (GRP78) and C/EBP homologous protein (CHOP) were increased [1]. In a transaortic constriction mice model, cardiac hypertrophy and dysfunction were attenuated in CHOP knockout mice compared with the wild type [2] In Akita diabetic mice, mRNA levels of GRP78/CHOP are increased, and deletion of CHOP delays the onset of diabetes. In these processes, ERS can lead to apoptosis.
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