Abstract
Low-level laser therapy (LLLT) has been used as an anti-inflammatory treatment in several disease conditions, even when inflammation is a secondary consequence, such as in myocardial infarction (MI). However, the mechanism by which LLLT is able to protect the remaining myocardium remains unclear. The present study tested the hypothesis that LLLT reduces inflammation after acute MI in female rats and ameliorates cardiac function. The potential participation of the Renin-Angiotensin System (RAS) and Kallikrein-Kinin System (KKS) vasoactive peptides was also evaluated. LLLT treatment effectively reduced MI size, attenuated the systolic dysfunction after MI, and decreased the myocardial mRNA expression of interleukin-1 beta and interleukin-6 in comparison to the non-irradiated rat tissue. In addition, LLLT treatment increased protein and mRNA levels of the Mas receptor, the mRNA expression of kinin B2 receptors and the circulating levels of plasma kallikrein compared to non-treated post-MI rats. On the other hand, the kinin B1 receptor mRNA expression decreased after LLLT. No significant changes were found in the expression of vascular endothelial growth factor (VEGF) in the myocardial remote area between laser-irradiated and non-irradiated post-MI rats. Capillaries density also remained similar between these two experimental groups. The mRNA expression of the inducible nitric oxide synthase (iNOS) was increased three days after MI, however, this effect was blunted by LLLT. Moreover, endothelial NOS mRNA content increased after LLLT. Plasma nitric oxide metabolites (NOx) concentration was increased three days after MI in non-treated rats and increased even further by LLLT treatment. Our data suggest that LLLT diminishes the acute inflammation in the myocardium, reduces infarct size and attenuates left ventricle dysfunction post-MI and increases vasoactive peptides expression and nitric oxide (NO) generation.
Highlights
The renin-angiotensin system (RAS) plays a pivotal role in the pathophysiology of myocardial infarction (MI), and in the development of heart failure [1]
The circulating levels of plasma kallikrein markedly increase after laser irradiation. (iv) level laser therapy (LLLT) fails to increase either capillaries density or vascular endothelial growth factor (VEGF) protein content in the remote area of MI. (v) whereas a diminished inducible nitric oxide synthase (iNOS) mRNA content is observed after LLLT, eNOS mRNA content and plasma nitric oxide metabolites (NOx) concentration are remarkably increased after LLLT, suggesting that nitric oxide (NO) generation may participate of the cardioprotective mechanism elicited by LLLT
This observation, taken together with the reduced mRNA content of IL-1beta and IL-6 in the MI+Laser group, suggests that the LLLT is effective to downregulating inflammatory mediators mRNA expression after MI as previously described [44]
Summary
The renin-angiotensin system (RAS) plays a pivotal role in the pathophysiology of myocardial infarction (MI), and in the development of heart failure [1]. Found in the systemic circulation, Ang-II is produced in the cardiac tissue by a local RAS [3]. Ang-II has been shown to increase oxidative stress, which could in turn activate inflammatory [4] and apoptotic [5] pathways. RAS blockade with ACE inhibitors (ACEis) or angiotensin receptor blockers (ARBs) has been shown to ameliorate several pathological cardiac conditions. This molecular suppression improves the outcome of cardiac remodeling [6,7,8,9]. A vasoactive system, the kallikrein-kinin system (KKS), is produced locally in the cardiac muscle.
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