Key result
In a rat model of coronary microembolization, pretreatment with the ERK1/2 inhibitor PD98059 significantly improved left ventricular ejection fraction compared to CME alone (76.46% vs 72.97%, p<0.05).
Why the study?
Does PD98059 improve cardiac function and reduce myocardial inflammation in a rat model of coronary microembolization?
Population
45 Sprague-Dawley rats in a model of coronary microembolization produced by injection of 42-μm microspheres…
Comparison
PD98059 injected 30 min before the CME operation. vs CME operation without PD98059, and sham-operated…
Design
Preclinical, randomly divided into three groups
Authors
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May support ERK1/2 inhibition in coronary microembolization models; leaves open translation to clinical disease.
Does PD98059 improve cardiac function and reduce myocardial inflammation in a rat model of coronary microembolization?
Absolute Event Rate: 76.46% vs 72.97%
p-value: p=<0.05
Inhibition of the ERK1/2 signaling pathway with PD98059 ameliorates myocardial inflammation and cardiac dysfunction in a rat model of coronary microembolization.
Li et al. (2010) studied Coronary microembolization-induced myocardial injury (n=45). PD98059 vs. CME alone and sham operation was evaluated on Left ventricular ejection fraction (LVEF) (p=<0.05). In a rat model of coronary microembolization, pretreatment with the ERK1/2 inhibitor PD98059 significantly improved left ventricular ejection fraction compared to CME alone (76.46% vs 72.97%, p<0.05).
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