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Cardiac shock wave therapy attenuates H9c2 myoblast apoptosis by activating the AKT signal pathway
Insights
Cardiac Shock Wave Therapy (CSWT) reduces apoptosis and cell death in heart cells experiencing ischemia/hypoxia. This therapy protects heart function by inhibiting the intrinsic apoptotic pathway and activating the PI3K-Akt pathway.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Biomedical Engineering
Background:
- Cardiac Shock Wave Therapy (CSWT) shows promise in improving myocardial perfusion and cardiac function in models of ischemia and in patients with coronary artery disease (CAD).
- Apoptosis is a critical factor in the pathogenesis of myocardial ischemia, but CSWT's effect on ischemia/hypoxia (I/H)-induced apoptosis and its underlying mechanisms remain unclear.
- This study investigates the hypothesis that CSWT protects heart function during I/H by reducing apoptosis.
Purpose of the Study:
- To determine if CSWT can protect against ischemia/hypoxia (I/H)-induced apoptosis in myocardial cells.
- To elucidate the molecular mechanisms by which CSWT exerts its protective effects.
- To investigate the potential role of the PI3K-Akt pathway in CSWT's cardioprotective action.
Main Methods:
- Ischemia/hypoxia (I/H)-induced apoptosis was established in the H9c2 myoblast cell line.
- Cells were treated with varying intensities of CSWT under I/H conditions.
- Apoptosis rates, cell viability, nuclear fragmentation, and the expression of apoptosis-related proteins (Bax, Bcl-2, Caspase3) were assessed. Activation of the PI3K-Akt pathway was also evaluated.
Main Results:
- CSWT effectively attenuated I/H-induced cell death and reduced the apoptosis rate in H9c2 cells.
- CSWT suppressed the expression of key molecules involved in the intrinsic apoptotic pathway.
- CSWT treatment led to increased phosphorylation of AKT, indicating activation of the PI3K-Akt signaling pathway.
Conclusions:
- CSWT demonstrates a protective effect against I/H-induced cell death by inhibiting the mitochondrial-dependent intrinsic apoptotic pathway.
- The PI3K-Akt signaling pathway is implicated as a potential mediator of CSWT's anti-apoptotic effects in the context of myocardial I/H.
- These findings suggest CSWT as a potential therapeutic strategy for conditions involving myocardial apoptosis.
Background:
Previous studies have demonstrated that Cardiac Shock Wave Therapy (CSWT) improves myocardial perfusion and cardiac function in a porcine model of chronic myocardial ischemia and also ameliorates myocardial ischemia in patients with severe coronary artery disease (CAD). Apoptosis plays a key role in ischemic myocardial pathogenesis. However, it remains unclear whether CSWT is beneficial for ischemia/hypoxia (I/H)-induced myocardial cell apoptosis and by which mechanism CSWT could improve heart function. We put forward the hypothesis that CSWT might protect heart function during ischemia/hypoxia by decreasing apoptosis.
Methods:
We generated ischemia/hypoxia (I/H)-induced apoptosis in the H9c2 myoblast cell line to examine the CSWT function and possible mechanisms. H9c2 cells were treated under hypoxic serum-starved conditions for 24 h and then treated with or without CSWT (500 shots, 0.06, 0.09, 0.12mJ/mm(2)). The apoptotic cell rate was determined by flow cytometry assay, cell viability was examined by the MTT assay, nuclear fragmentation was detected by Hoechst 33342 staining, and the mitochondrial-mediated intrinsic pathway of apoptosis was assessed by the expression of Bax and Bcl-2 protein and Caspase3 activation.
Results:
First, apoptosis could be induced by ischemia/hypoxia in H9c2 cells. Second, CSWT attenuates the cell death and decreases the H9c2 cell apoptosis rate induced by ischemia and hypoxia. Third, CSWT suppresses the expression of apoptosis molecules that regulate the intrinsic pathway of apoptosis in H9c2 cells. Fourth, CSWT increases the phosphorylation of AKT, which indicates the activation of the PI3K-AKT pathway.
Conclusions:
These results indicate that CSWT exerts a protective effect against I/H-induced cell death, potentially by preventing the activation of components of the mitochondrial-dependent intrinsic apoptotic pathway. We also demonstrate that the PI3K-Akt pathway may be involved in the CSWT effects on apoptosis.
