Inflammation is a pivotal feature of myocardial reperfusion–induced microvascular injury and dysfunction. However, the molecular mechanisms by which myocardial reperfusion triggered inflammation remain incurable. The NLRP3 inflammasome is a key intracellular sensor that detection of cellular stress to activation of caspase-1, and consequent IL-1β maturation and pyroptotic cell death. Here, we showed that NLRP3 inflammasome played a key role in myocardial reperfusion–induced microvascular injury. We observed NLRP3 inflammasome activation and pyroptosis in both cardiac microvascular endothelial cells and myocardial I/R animal model. Gastrodin, an effective monomeric component extracted from the herb Gastrodia elata BIume, blocked cardiac microvascular endothelial cell pyroptosis via inhibiting NLRP3/caspase-1 pathway. Gastrodin also reduced interleukin-1β (IL-1β) production in vivo and in vitro. Furthermore, gastrodin treatment attenuated infarct size and inflammatory cells infiltration and increased capillary formation. Gastrodin is thus a potential therapeutic for NLRP3-associated inflammatory disease.

中文翻译：

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天麻素可通过调节NLRP3 / caspase-1途径改善微血管再灌注损伤引起的细胞凋亡。

炎症是心肌再灌注引起的微血管损伤和功能障碍的关键特征。但是，心肌再灌注引发炎症的分子机制仍然无法治愈。NLRP3炎性小体是关键的细胞内传感器，可检测细胞对激活caspase-1的压力，进而检测IL-1β的成熟和凋亡的细胞死亡。在这里，我们表明NLRP3炎性小体在心肌再灌注引起的微血管损伤中发挥了关键作用。我们在心脏微血管内皮细胞和心肌I / R动物模型中均观察到NLRP3炎性小体激活和焦磷酸化。天麻素是一种从草本天麻中提取的有效单体成分，它通过抑制NLRP3 / caspase-1途径阻断了心脏微血管内皮细胞的热凋亡。。此外，天麻素处理可减轻梗塞面积和炎性细胞浸润并增加毛细血管形成。天麻素因此是与NLRP3相关的炎性疾病的潜在治疗剂。