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Shows that NLRP3 inflammasome-driven pyroptosis worsens myocardial ischemia-reperfusion injury in diabetic rats, indicating that blocking this pathway could protect the diabetic heart.
The reactive oxygen species‐ (ROS‐) induced nod‐like receptor protein‐3 (NLRP3) inflammasome triggers sterile inflammatory responses and pyroptosis, which is a proinflammatory form of programmed cell death initiated by the activation of inflammatory caspases. NLRP3 inflammasome activation plays an important role in myocardial ischemia/reperfusion (MI/R) injury. Our present study investigated whether diabetes aggravated MI/R injury through NLRP3 inflammasome‐mediated pyroptosis. Type 1 diabetic rat model was established by intraperitoneal injection of streptozotocin (60 mg/kg). MI/R was induced by ligating the left anterior descending artery (LAD) for 30 minutes followed by 2 h reperfusion. H9C2 cardiomyocytes were exposed to high glucose (HG, 30 mM) conditions and hypoxia/reoxygenation (H/R) stimulation. The myocardial infarct size, CK‐MB, and LDH release in the diabetic rats subjected to MI/R were significantly higher than those in the nondiabetic rats, accompanied with increased NLRP3 inflammasome activation and increased pyroptosis. Inhibition of inflammasome activation with BAY11‐7082 significantly decreased the MI/R injury. In vitro studies showed similar effects, as BAY11‐7082 or the ROS scavenger N‐acetylcysteine, attenuated HG and H/R‐induced H9C2 cell injury. In conclusion, hyperglycaemia‐induced NLRP3 inflammasome activation may be a ROS‐dependent process in pyroptotic cell death, and NLRP3 inflammasome‐induced pyroptosis aggravates MI/R injury in diabetic rats.
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Qiu et al. (2017) studied this question.
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