Abstract
Myocardial infarction triggers massive biochemical changes, even cardiac cell death. Endoplasmic reticulum stress is involved in the pathology of myocardial infarction-mediated apoptosis. In the present study, myocardial cell line H9c2 cells were treated with cobalt chloride (CoCl2) to induce hypoxia. Isoproterenol was used for two successive days to induce myocardial infarction in SD rats. The cardioprotective effect of olive leaf extract (OLE) and its main constituent hydroxytyrosol and the underlying mechanisms were evaluated. The results showed that hydroxytyrosol markedly protected H9c2 cells against CoCl2-induced apoptosis. Hydroxytyrosol could reduce the mRNA and protein expression of GRP78 and CHOP induced by CoCl2 in vitro. In vivo, the decreased ejection fraction and fractional shortening, increased heart weight/body ratio, the formation of infarction, disordered cardiac muscle fibers and infiltration of inflammatory cells induced by isoproterenol could be significantly ameliorated by pretreatment with OLE for a month. Similarly, OLE could also reverse the increase of GRP78 and CHOP expression induced by isoproterenol. Therefore, OLE and hydroxytyrosol exert a cardioprotective effect through endoplasmic reticulum stress, which could be a new target for the prevention and treatment of cardiovascular diseases.
Highlights
Myocardial infarction (MI) leads to heart failure and subsequent death[1]
We investigated the protective effect of olive leaf extract (OLE) on MI induced by isoprenaline in vivo, and the protective effect of hydroxytyrosol on cardiomyocyte H9c2 induced by CoCl2 in vitro through the endoplasmic reticulum (ER) stress pathway
Similar results were observed in the protein expression. These results demonstrated that the protection of OLE against isoproterenol-induced MI in vivo involved the inhibition of GRP78 and C/EBP homologous protein (CHOP) expression
Summary
Myocardial infarction (MI) leads to heart failure and subsequent death[1]. It is still a main cause of death in the world despite advances in treatments[2–3]. Studies have shown that endoplasmic reticulum (ER) stress in cardiomyocytes can generate and promote cell apoptosis[4]. The C/EBP homologous protein (CHOP) pathway is the major signal pathway through which ER stress induces apoptosis. GRP78, one kind of heat shock protein 70, is the main protein in the CHOP pathway[5]. The expression of heat shock proteins is an essential way to antagonize this stress[6]. Studies have shown that GRP78 responds to hypoxia and ischemia effectively[7]. CHOP and GRP78 have been widely used as specific markers for ER stress[8]
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