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Salvianolic acid B (SalB), produced by Radix Salviae, exerts antioxidative and anti\u2010inflammatory activities in multiple cell types. However, SalB\u2019s effects on ER stress\u2010related inflammasome and endothelial dysfunction remain unknown. Here, we showed SalB substantially abrogated ER stress\u2010induced cell death and reduction in capillary tube formation, with declined intracellular reactive oxygen species (ROS) amounts and restored mitochondrial membrane potential (MMP), as well as increased expression of HO\u20101 and SOD2 in bone marrow\u2010derived endothelial progenitor cells (BM\u2010EPCs). ER stress suppression by CHOP or caspase\u20104 siRNA transfection attenuated the protective effect of SalB. Additionally, SalB alleviated ER stress\u2010mediated pyroptotic cell death via the suppression of TXNIP\/NLRP3 inflammasome, as evidenced by reduced cleavage of caspase\u20101 and interleukin\u2010 (IL\u2010) 1<jats:italic>\u03b2<\/jats:italic> and IL\u201018 secretion levels. Furthermore, this study provided a mechanistic basis that AMPK\/FoxO4\/KLF2 and Syndecan\u20104\/Rac1\/ATF2 signaling pathway modulation by SalB substantially prevented BM\u2010EPCs damage associated with ER stress by decreasing intracellular ROS amounts and inducing NLRP3\u2010dependent pyroptosis. In summary, our findings identify that ER stress triggered mitochondrial ROS release and NLRP3 generation in BM\u2010EPCs, while SalB inhibits NLRP3 inflammasome\u2010mediated pyroptotic cell death by regulating the AMPK\/FoxO4\/KLF2 and Syndecan\u20104\/Rac1\/ATF2 pathways. The current findings reveal SalB as a potential new candidate for the treatment of atherosclerotic heart disease.<\/jats:p>","DOI":"10.1155\/2022\/8332825","type":"journal-article","created":{"date-parts":[[2022,3,17]],"date-time":"2022-03-17T23:35:21Z","timestamp":1647560121000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":47,"title":["Salvianolic Acid B Suppresses ER Stress\u2010Induced NLRP3 Inflammasome and Pyroptosis via the AMPK\/FoxO4 and Syndecan\u20104\/Rac1 Signaling Pathways in Human Endothelial Progenitor 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