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Published on: August 3, 2018
Coronary microembolization induced myocardial contractile dysfunction and tumor necrosis factor-α mRNA expression
1Department of Cardiology, First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021, China. drlilang@163.com
Background:
The microemboli produced during spontaneous plaque rupture and ulceration and during coronary intervention will reduce coronary reserve and cause cardiac dysfunction. It is though that inflammation caused by the microinfarction induced by the microembolization may play an essential role. It is known that the activation of p38 mitogen-activated protein kinases (MAPK) in both infected and non-infected inflammation in myocardium may cause a contractile dysfunction. But the relation between the activation of p38 MAPK and microembolization is still unknown.
Methods:
Sprague-Dawley rats were randomly divided into three groups: Sham group, coronary microembolization (CME) group and SB203580 group (n = 10 per group). CME rats were produced by injection of 42 µm microspheres into the left ventricle with occlusion of the ascending aorta. SB203580, a p38 MAPK inhibitor, was injected into the femoral vein after the injection of microspheres to make the SB203580 group. Left ventricular ejection fraction (LVEF) was determined by echocardiography. The protein concentration of P38 MAPK in the myocardium was assessed by Western blotting. The relative expression of mRNA for tumor necrosis factor (TNF)-α was assessed by the technique of semi-quantitative polymerase chain reaction amplification.
Results:
LVEF was depressed at three hours up to 12 hours in the CME group. Increased p38 MAPK activity and TNF-α mRNA expression were observed in the CME group. The administration of SB203580 partly inhibited p38 MAPK activity, but did not fully depress the TNF-α expression, and partly preserved cardiac contractile function.
Conclusions:
p38 MAPK is significantly activated by CME and the inhibition of p38 MAPK can partly depress the TNF-α expression and preserve cardiac contractile function.
Insights
Coronary microembolization activates p38 MAPK, leading to cardiac dysfunction. Inhibiting p38 MAPK partially reduces inflammation and preserves heart function, suggesting a therapeutic target for microembolization.
Area of Science:
- Cardiology
- Molecular Biology
- Inflammation Research
Background:
- Microemboli from plaque rupture or interventions impair cardiac function.
- Inflammation, potentially mediated by p38 MAPK, is implicated in microinfarction-induced cardiac dysfunction.
- The link between p38 MAPK activation and microembolization remains unclear.
Purpose of the Study:
- To investigate the role of p38 MAPK activation in cardiac dysfunction following coronary microembolization (CME).
- To evaluate the therapeutic potential of inhibiting p38 MAPK in CME-induced cardiac dysfunction.
Main Methods:
- Coronary microembolization induced in rats using microspheres.
- Administration of SB203580, a p38 MAPK inhibitor, to assess its effects.
- Assessment of left ventricular ejection fraction (LVEF) via echocardiography.
- Measurement of myocardial p38 MAPK protein and TNF-α mRNA expression.
Main Results:
- CME significantly reduced LVEF for up to 12 hours.
- p38 MAPK activity and TNF-α mRNA expression increased in CME rats.
- SB203580 partially inhibited p38 MAPK and TNF-α, preserving cardiac function.
Conclusions:
- p38 MAPK is activated by coronary microembolization.
- Inhibiting p38 MAPK offers partial protection against CME-induced cardiac dysfunction and inflammation.
