Key result
Carvedilol administration significantly reduced myocardial infarction-induced cardiomyocyte apoptosis in rats by up to 36%, likely through the down-regulation of TLR4 and NF-κB expression.
Why the study?
Does carvedilol reduce cardiomyocyte apoptosis in a rat model of myocardial infarction?
Population
48 rats, randomized to sham-operated, myocardial infarction group, and three carvedilol-treatment groups. MI…
Comparison
Carvedilol administered by direct gastric gavage… vs Vehicle administered by direct gastric gavage…
Design
Preclinical, randomized to the following groups before surgery, The assays…
Follow-up
3 days after MI
Authors
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No immediate clinical implications for MI care; leaves open translation of anti-apoptotic effects from rat models to humans.
Does carvedilol reduce cardiomyocyte apoptosis in a rat model of myocardial infarction?
Effect estimate: 36% maximal inhibition
p-value: p=<0.05
Carvedilol reduces cardiomyocyte apoptosis in a rat model of myocardial infarction, potentially through the inhibition of TLR4 and NF-κB signaling pathways.
Xu et al. (2013) studied Myocardial infarction (n=48). Carvedilol vs. Vehicle was evaluated on Percentage of TUNEL-positive apoptotic cardiomyocytes (36% maximal inhibition, p=<0.05). Carvedilol administration significantly reduced myocardial infarction-induced cardiomyocyte apoptosis in rats by up to 36%, likely through the down-regulation of TLR4 and NF-κB expression.
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