Figure 9.

PS inhibit the NLRP3 inflammasome through two different pathways. To activate the NLRP3 inflammasome, NF-κB was stimulated in the early stage (1 h after treatment with LPS/ATP) and ER stress was stimulated in the late stage (12 h after treatment with LPS/ATP); both pathways enhanced Ca²⁺ accumulation and the subsequent mtROS generation, which lead to IL-1β and IL-18 release. PS inhibited the NF-κB signaling pathway in the early stage and downregulated ER stress in the late stage, which reduced intracellular Ca²⁺-mediated mtROS production and subsequently inhibited NLRP3 inflammasome-induced IL-1β and IL-18 release. NLRP3: NOD, LRR, and pyrin domain-containing protein 3; NF-κB: nuclear factor-κB; ER: endoplasmic reticulum; mtROS: mitochondrial reactive oxygen species.