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Front Pharmacol. 2017 Jul 11;8:456. doi: 10.3389/fphar.2017.00456. eCollection 2017.

Rosmarinic Acid Protects against Inflammation and Cardiomyocyte Apoptosis during Myocardial Ischemia/Reperfusion Injury by Activating Peroxisome Proliferator-Activated Receptor Gamma.

Author information

1
School of Integrated Traditional Chinese and Western Medicine, Binzhou Medical UniversityYantai, China.
2
State Key Laboratory of Natural Medicines, China Pharmaceutical UniversityNanjing, China.
3
Department of Cardiac Surgery, Shandong Provincial Qianfoshan Hospital, Shandong UniversityJinan, China.
4
College of Arts and Sciences, Shanxi Agricultural UniversityTaigu, China.
5
Key Laboratory of Xinjiang Endemic Phytomedicine Resources, Ministry of Education, School of Pharmacy, Shihezi UniversityShihezi, China.

Abstract

The cardiac ischemia-reperfusion (I/R) injury greatly influences the therapeutic effect and remains an urgent challenge in clinical therapy. Polypharmacology opens a new therapeutic opportunity to design drugs with a specific target for improving the efficacy. In this study, we first forecasted that Rosmarinic acid (RosA) could be used for the treatment of cardiovascular disease using text mining, chemometric and chemogenomic methods. Consistent with the effect of the positive drug (pioglitazone, PIO), we subsequently validated that RosA pretreatment could restore the decreased cardiac hemodynamic parameters (LVDP, ± dp/dtmin, ± dp/dtmax and CF), decreased the infarct size and the cardiomyocyte apoptosis in a rat model of cardiac I/R injury. Furthermore, RosA pre-treatment inhibited the levels of inflammatory cytokines (IL-6, TNF-α and CRP), up-regulated PPARγ expression and down-regulated NF-κB expression in myocardial tissue isolated from the rat model of I/R-induced myocardial injury. In addition, the effects of RosA were reversed by co-treatment with PPAR-γ inhibitor GW9662 and T0070907, respectively. These data suggest that RosA attenuates cardiac injury through activating PPARγ and down-regulating NF-κB-mediated signaling pathway, which inhibiting inflammation and cardiomyocyte apoptosis in a rat model of cardiac I/R injury.

KEYWORDS:

NF-κB p65; PPARγ; Rosmarinic acid; cardio-protection; ischemia/reperfusion

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