Taurine Alleviates Sympathetic Innervation by Inhibiting NLRP3 Inflammasome in Post‐infarcted Rats

The NLRP3 inflammasome is activated by myocardial infarction, and then induces the activation of inflammatory caspase‐1 activation and maturation of IL‐1β, a regulator of synthesis of nerve growth factor (NGF). Here, we studied whether taurine, 2‐aminoethanesulphonic acid, can attenuate cardiac sympathetic reinnervation by modulating NLRP3 inflammasome‐mediated NGF in a rat model of myocardial infarction. Male Wistar rats were subjected to coronary ligation and then randomized to either saline or taurine for 3 days or 4 weeks. Postinfarction was associated with activation of NF‐kB (p65) and NLRP3 inflammasome component and increased the protein and expression of IL‐1β. Macrophages at the border zone were shown to be positive for IL‐1β 3 days postinfarction. Compared with vehicle, infarcted rats treated with taurine significantly attenuated myocardial mRNA and protein levels of NF‐kB, NLRP3 inflammasome, mature caspase‐1 and IL‐1β. Immunofluorescent analysis, real‐time quantitative RT–PCR, and Western blotting of NGF showed that sympathetic hyperinnervation was blunted after administering taurine. Arrhythmia vulnerability in the taurine‐treated infarcted rats was significantly improved than those in vehicle. Ex vivo studies showed that taurine infusion reduced myocardial IL‐1β level at the extent similar to either PDTC or CP‐456,773, inhibitors of NF‐kB and NLRP3 inflammasome, implying the key axis of NF‐kB/NLRP3 inflammasome in mediating taurine‐related anti‐inflammation. Furthermore, administration of anti‐IL‐1β antibody reduced NGF levels. Taurine attenuated sympathetic innervation mainly via NLRP3 inflammasome/IL‐1β‐dependent pathway, which downregulated expression of NGF in infarcted rats. These findings may provide a new insight into the anti‐inflammation effect of taurine.