Light-emitting diode therapy protects against ventricular arrhythmias by neuro-immune modulation in myocardial ischemia and reperfusion rat model

发光二极管疗法通过神经免疫调节预防心肌缺血再灌注大鼠模型中的室性心律失常

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作者:Songyun Wang, Lin Wu, Xuemeng Li, Binxun Li, Yi Zhai, Dongdong Zhao, Hong Jiang

Background

Sympathetic overactivation and inflammation are two major mediators to post-myocardial ischemia-reperfusion (I/R)-induced ventricular arrhythmia (VA). The vicious cycle between microglia and sympathetic activation plays an important role in sympathetic hyperactivity related to cardiovascular diseases. Recently, studies have shown that microglial activation might be attenuated by light-emitting diode (LED) therapy. Therefore, we hypothesized that LED therapy might protect against myocardial I/R-induced VAs by attenuating microglial and sympathetic activation.

Conclusions

LED therapy may protect against myocardial I/R-induced VAs by central and peripheral neuro-immune regulation.

Methods

Thirty-six male anesthetized rats were randomized into four groups: control group (n = 6), LED group (n = 6), I/R group (n = 12), and LED+I/R group (n = 12). I/R was generated by left anterior descending artery occlusion for 30 min followed by 3 h reperfusion. ECG and left stellate ganglion (LSG) neural activity were recorded continuously. After 3 h reperfusion, a programmed stimulation protocol was conducted to test the inducibility of VA. Furthermore, we extracted the brain tissue to examine the microglial activation, and the peri-ischemic myocardium to examine the expression of NGF and inflammatory cytokines (IL-1β, IL-18, IL-6, and TNF-α).

Results

As compared to the I/R group, LED illumination significantly inhibited the LSG neural activity (P < 0.01) and reduced the inducibility of VAs (arrhythmia score 4.417 ± 0.358 vs. 3 ± 0.3257, P < 0.01) in the LED+I/R group. Furthermore, LED significantly attenuated microglial activation and downregulated the expression of inflammatory cytokines and NGF in the peri-infarct myocardium. Conclusions: LED therapy may protect against myocardial I/R-induced VAs by central and peripheral neuro-immune regulation.

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