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

Abstract

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. 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.

Silenced SOX2‐OT alleviates ventricular arrhythmia associated with heart failure by inhibiting NLRP3 expression via regulating miR‐2355‐3p

“…Caspase‐1 NLRP3 and ASC are components of NLRP3 inflammasomes that can cause cardiac inflammation and cardiac dysfunction via IL‐1β and TGF‐β1 release 13–16 . Inhibiting TGF‐β and IL‐1β expression can alleviate cardiac dysfunction in ischemic VA‐HF 9–11 . The present study found that NLRP3 inflammasomes and the expression of IL‐1β and TGF‐β1 gradually increased in healthy rats, and in rats with HF and VA‐HF.…”

“…IL‐1β aggravates VA induced by ischemia 8 . Inhibiting the expression of TGF‐β, IL‐1β, IL‐6, IL‐18, and TNF‐α can reduce VA in ischemic HF, which plays a role in anti‐VA 9–11 . Nucleotide‐binding oligomerization domain‐like receptor family pyrin domain containing 3 (NLRP3) inflammasomes were recently discovered as inflammatory response regulators that consist of NLRP3, ASC, and caspase‐1.…”

Non-invasive Autonomic Neuromodulation Is Opening New Landscapes for Cardiovascular Diseases

“…LED therapy might reduce myocardial ischemia/reperfusion-induced ventricular arrhythmias by attenuating microglial and sympathetic over-activation. They also proved that LED therapy has the same indirect effects of sympathetic activity in a rat model of acute myocardial ischemia/reperfusion injury (Wang et al, 2019c). This indicates that LED affects the ANS through the inhibition of inflammation rather than through direct effects.…”

MicroRNA-668-3p Protects Against Oxygen-Glucose Deprivation in a Rat H9c2 Cardiomyocyte Model of Ischemia-Reperfusion Injury by Targeting the Stromal Cell-Derived Factor-1 (SDF-1)/CXCR4 Signaling Pathway

“…Also, there is an association between obesity and inflammation [12]. A recent study showed that light-emitting diode (LED) therapy protected against myocardial IRI-induced ventricular arrhythmia by suppressing microglial activation and the expression of inflammatory cytokines in the ischemic myocardium [26]. Salahshoor et al showed that royal jelly had antioxidant and anti-inflammatory properties that reduced IRI-induced renal injury [27].…”