Abstract
Objective: This study aimed to investigate the effect of osmotin on myocardial ischemia/reperfusion (I/R), as well as the underlying mechanisms.Methods: In vitro I/R injury model was established on rat cardiac myoblast H9c2 cells by oxygen and glucose deprivation followed by reperfusion (OGD/R). Cells were administrated with osmotin, and transfected with small interfering RNAs (siRNAs) which specifically target adiponectin receptor 1 or 2 (AdipoR1/2). Besides, the cells were incubated with or without LY294002 as inhibitor of phosphatidylinositol 3-kinase (PI3K) under OGD/R condition. Cell viability, apoptosis, expressions of apoptosis-related proteins and inflammatory factors were analyzed.Results: The results showed that osmotin significantly increased H9c2 cells viability compared with the cells treated with vehicle (P < 0.05), and decreased H9c2 cells apoptosis by regulating expressions of apoptosis-related proteins. Moreover, we observed that osmotin statistically reduced the release of proinflammatory factors and increased the release of anti-inflammatory factors in H9c2 cells (P < 0.05). However, these effects were markedly reversed by AdipoR1 silence but not AdipoR2. Furthermore, osmotin dramatically upregulated the phosphorylation levels of PI3K, AKT, ERK, and downregulated the phosphorylation level of NF-κB (P < 0.05). While administration of LY294002 reduced cell viability, increased cell apoptosis, and aggravated inflammatory response (P < 0.05).Conclusion: Our results suggested that the protective effect of osmotin on the simulated OGD/R injured H9c2 cells might be associated with AdipoR1/PI3K/AKT signaling pathway.
Highlights
Acute myocardial infarction (AMI) is a common and lethal heart disease which threatens people’s life worldwide (SantosGallego et al, 2014)
The results showed that osmotin significantly increased H9c2 cells viability compared with the cells treated with vehicle (P < 0.05), and decreased H9c2 cells apoptosis by regulating expressions of apoptosis-related proteins
Our results suggested that the protective effect of osmotin on the simulated oxygen and glucose deprivation followed by reperfusion (OGD/R) injured H9c2 cells might be associated with AdipoR1/phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway
Summary
Acute myocardial infarction (AMI) is a common and lethal heart disease which threatens people’s life worldwide (SantosGallego et al, 2014). Reperfusion is critical for the salvage of ischemic myocardium. Reperfusion was well acknowledged to protect the ischemic myocardium against inevitable death, it has side effect which was called ischemia/reperfusion (I/R) injury (Heusch, 2013). Myocardial I/R injury is a very complex pathophysiological process that can lead to serious acute and chronic myocardial damage. In addition to cell necrosis, cell apoptosis is another important cause which induce cell death during myocardial I/R. It has been well demonstrated that a cascade of acutely initiated local inflammatory responses were one of the most important pathological processes during I/R (Frangogiannis et al, 2002; Kawaguchi et al, 2011). Reduction of cell apoptosis and inflammatory responses might be of great importance
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