Gastrodin ameliorates microvascular reperfusion injury–induced pyroptosis by regulating the NLRP3/caspase-1 pathway
- Autores: Wenjing Sun, Hongquan Lu, Lechun Lyu, Ping Yang, Zhi Lin, Ling Li, Lin Sun, Di Lu
- Localización: Journal of physiology and biochemistry, ISSN-e 1877-8755, ISSN 1138-7548, Vol. 75, Nº. 4, 2019, págs. 531-547
- Idioma: inglés
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Resumen
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.
