The Cardioprotective Effect of Protocatechuic Acid on Myocardial Ischemia/Reperfusion Injury

Protocatechuic acid (PCA), a phenolic compound and one of the main metabolites of complex polyphenols, has been found to possess various biological activities, and it may have a potential in the treatment of ischemic heart diseases. This study explored the cardioprotective effect of PCA on myocardia...

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Bibliographic Details
Published in:Journal of Pharmacological Sciences 2014/06/20, Vol.125(2), pp.176-183
Main Authors: Tang, Xi-Lan, Liu, Jian-Xun, Dong, Wei, Li, Peng, Li, Lei, Lin, Cheng-Ren, Zheng, Yong-Qiu, Cong, Wei-Hong, Hou, Jin-Cai
Format: Article
Language:English
Subjects:
Animals
apoptosis
Apoptosis - drug effects
Cardiotonic Agents
Caspase 3 - metabolism
Cells, Cultured
Disease Models, Animal
Hydroxybenzoates - pharmacology
Hydroxybenzoates - therapeutic use
inflammatory response
Male
Myocardial Ischemia - blood
Myocardial Ischemia - drug therapy
Myocardial Ischemia - pathology
myocardial ischemia/reperfusion injury
Myocardial Reperfusion Injury - blood
Myocardial Reperfusion Injury - drug therapy
Myocardial Reperfusion Injury - pathology
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - pathology
platelet aggregation
Platelet Aggregation - drug effects
Proto-Oncogene Proteins c-akt - metabolism
protocatechuic acid
Rats, Sprague-Dawley
Rats, Wistar
Tumor Necrosis Factor-alpha - blood
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Summary:Protocatechuic acid (PCA), a phenolic compound and one of the main metabolites of complex polyphenols, has been found to possess various biological activities, and it may have a potential in the treatment of ischemic heart diseases. This study explored the cardioprotective effect of PCA on myocardial ischemia/reperfusion (MI/R) injury and the underlying mechanisms. In an in vivo rat model of MI/R injury, myocardial infarct size, serum TNF-α level, and platelet aggregation were measured. In a primary neonatal rat cardiomyocyte model of hypoxia/ reoxygenation (H/R) injury, the apoptotic rate, expressions of cleaved caspase-3, and phosphorylated Akt were observed. We found that PCA significantly reduced myocardial infarct size, serum TNF-α level, and platelet aggregation. In vitro experiments revealed that PCA significantly inhibited the apoptotic rate and the expression of cleaved caspase-3, and it upregulated the expression of phosphorylated Akt in cardiomyocytes subjected to H/R injury. Our results suggest that PCA can provide a significant protection against MI/R injury, which may be at least partially attributed to its inhibitions against injury induced by MI/R including the inflammatory response, platelet aggregation, and cardiomyocytes apoptosis. [Supplementary Figures: available only at http://dx.doi.org/10.1254/jphs.13247FP]
ISSN:1347-8613
1347-8648
DOI:10.1254/jphs.13247FP