Protective Effect of RA on Myocardial Infarction-Induced Cardiac Fibrosis via AT1R/p38 MAPK Pathway Signaling and Modulation of the ACE2/ACE Ratio

Cardioprotection Cardiac Fibrosis Hydroxyproline Angiotensin-converting enzyme 2
DOI: 10.1021/acs.jafc.6b03001 Publication Date: 2016-08-19T09:26:43Z
ABSTRACT
Rosmarinic acid (α-o-caffeoyl-3,4-dihydroxyphenyllactic acid, RA) is a major active constituent of Rosmarinus officinalis Linn. (rosemary) having significant anti-inflammatory, anti-apoptotic, and antioxidant effects. However, the cardioprotection RA still not understood. The present study was designed, for first time, to investigate on myocardial infarction (MI)-induced cardiac fibrosis clarify possible mechanisms. MI induced in adult rats by left anterior descending coronary artery ligation, animals were then administered (50, 100, or 200 mg/kg) gavage. Compared with model group, treatment ameliorated changes ventricular systolic pressure (LVSP), +dp/dtmax, -dp/dtmax after 4 weeks. This associated attenuation infarct size, collagen volume fraction (CVF), expression I, III, alpha smooth muscle actin (α-SMA), hydroxyproline (Hyp) concentrations. also decreased angiotensin-converting enzyme (ACE) increased ACE2 expression, as well angiotensin type 1 receptor (AT1R) phospho-p38 mitogen-activated protein kinase (p38 MAPK). Thus, can protect against dysfunction following MI, likely due decreasing ACE increasing via AT1R/p38 MAPK pathway.
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