Light Emitting Diode Therapy Protects against Myocardial Ischemia/Reperfusion Injury through Mitigating Neuroinflammation.

Songyun Wang,Lin Wu,Jingyu Huang,Binxun Li,Qinyu Luo,Dongdong Zhao,Hong Jiang,Hui Chen,Zhen Wang,Xuemeng Li

doi:10.1155/2020/9343160

Abstract

Background Neuroinflammation plays a key role in myocardial ischemia-reperfusion (I/R) injury. Previous studies showed that light-emitting diode (LED) therapy might improve M2 microglia activation and brain-derived neurotrophic factor (BDNF) expression, thereby exerting anti-inflammatory effects. Therefore, we hypothesized that LED therapy might reduce myocardial I/R injury by neuroinflammation modulation. Objective To explore the effect of LED therapy on myocardial I/R-induced injury and seek the underlying mechanism. Methods Thirty rats were randomly divided into three groups: Control group (without LED treatment or myocardial I/R, n = 6), I/R group (with myocardial I/R only, n = 12), and LED+I/R group (with myocardial I/R and LED therapy, n = 12). Electrocardiogram was recorded continuously during the procedure. In addition, brain tissue was extracted for BDNF, Iba1, and CD206 analyses, and heart tissue for myocardial injury (ischemic size and infarct size), IL-4 and IL-10 mRNA analysis. Results In comparison with the I/R group, the ischemia size and the infarct size were significantly attenuated by LED therapy in the LED+I/R group. Meanwhile, the microglia activation induced by I/R injury was prominently attenuated by LED treatment either. And it is apparent that there was also an increase in the beneficial neuroinflammation markers (BDNF and CD206) in the paraventricular nucleus (PVN) in the LED+I/R group. Furthermore, the anti-inflammatory cytokines, IL-4 and IL-10, were greatly decreased by I/R while improved by LED treatment in myocardium. Conclusion LED therapy might reduce neuroinflammation in PVN and decrease myocardium injury by elevating BDNF and M2 microglia.

Highlights

Myocardial infarction (MI) is a major cause for the sudden death of patients
The activation of microglia induced by myocardial I/R injury was significantly decreased by light-emitting diode (LED) therapy (30:1 ± 3:252% vs. 46:72 ± 3:18%, P < 0:01) (Figure 2(c))
CD206, which was known as a biomarker for the anti-inflammatory M2 type microglia, was remarkably decreased in the I/R group as compared that into the Control group (27:13 ± 2:51% vs. 43:74 ± 3:15%, P < 0:001), whereas

Summary

Introduction

Myocardial infarction (MI) is a major cause for the sudden death of patients. Currently, early successful blood restoring is the most effective approach for reducing the myocardial injury of patients with acute myocardial infarction (AMI). Reperfusion therapy itself can cause damage to myocardial cells and result in the myocardial injury, and no effective therapy for preventing this has been shown [1, 2]. Previous studies have shown that neuroinflammation in PVN, the cardiovascular regulatory center in the brain, was involved in many cardiovascular diseases such as myocardial infarction, myocardial I/R, and hypertension [3,4,5,6,7]. Previous studies showed that light-emitting diode (LED) therapy might improve M2 microglia activation and brain-derived neurotrophic factor (BDNF) expression, thereby exerting anti-inflammatory effects. We hypothesized that LED therapy might reduce myocardial I/R injury by neuroinflammation modulation. To explore the effect of LED therapy on myocardial I/R-induced injury and seek the underlying mechanism. LED therapy might reduce neuroinflammation in PVN and decrease myocardium injury by elevating BDNF and M2 microglia

Methods

Results

Discussion

Conclusion