Key result
Inhibition of IL-6 or the glycoprotein 130-STAT3 pathway in the paraventricular nucleus of MI rats increased vulnerability to ventricular arrhythmia.
Why the study?
The paraventricular nucleus is involved in malignant ventricular arrhythmia after acute myocardial infarction, but the underlying mechanisms remain incompletely understood.
The IL-6-Gp130-STAT3 pathway in the paraventricular nucleus exerts a protective effect against ventricular arrhythmias in a rat model of myocardial infarction.
Caution against IL-6 pathway inhibition post-MI; leaves open central anti-arrhythmic targets for translational study.
BACKGROUND: Malignant ventricular arrhythmia (VA) is the most common cause of death associated with acute myocardial infarction (MI). Recent studies have revealed direct involvement of the paraventricular nucleus (PVN) in the occurrence of VA. However, the underlying mechanisms remain incompletely understood. In this study, we investigated changes in the interleukin-6 (IL-6)-glycoprotein 130-signal transducer and activator of transcription 3 (STAT3) pathway in the PVN during acute MI and the effects of this pathway on ventricular stability. METHODS: Rats were divided into a control group, a MI group, a PVN-injected anti-IL-6 antibody group and a PVN-injected SC144 group to observe how IL-6 and its downstream glycoprotein 130-STAT3 pathway in the PVN affect ventricular stability. The left anterior descending coronary artery was ligated to induce MI. After that, an anti-IL-6 antibody and SC144 were injected into the PVNs of rats. All data are expressed as the mean ± SE and were analysed by ANOVA with a post hoc LSD test. p < 0.05 was considered to indicate statistical significance. RESULTS: After MI, the concentration of the inflammatory factor IL-6 increased, and its downstream glycoprotein 130-STAT3 pathway was activated in the PVN. After injection of MI rat PVNs with the anti-IL-6 antibody or glycoprotein 130 inhibitor (SC144), glutamate levels increased and γ-aminobutyric acid (GABA) levels decreased in the PVN. Plasma norepinephrine concentrations also increased after treatment, which increased the vulnerability to VA. CONCLUSIONS: In summary, IL-6 in the PVN exerts a protective effect in MI rats, and the glycoprotein 130-STAT3 pathway plays a key role in this process. We anticipate that our findings will provide new ideas for the prevention and treatment of arrhythmia after MI.
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Gao et al. (2020) studied Myocardial infarction. PVN-injected anti-IL-6 antibody or SC144 (glycoprotein 130 inhibitor) vs. Control group and MI group was evaluated on Vulnerability to ventricular arrhythmia and neurotransmitter levels. Inhibition of IL-6 or the glycoprotein 130-STAT3 pathway in the paraventricular nucleus of MI rats increased vulnerability to ventricular arrhythmia.
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