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Phillyrin, a principal bioactive compound from\n                      <jats:italic>Forsythia suspensa (Thunb.) Vahl<\/jats:italic>\n                      , has shown therapeutic promise in viral lung inflammation. However, its potential therapeutic effect and mechanism of action in KD-induced lung injury are entirely unexplored.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Aim of the study<\/jats:title>\n                    <jats:p>This study was designed to explore the therapeutic potential of phillyrin against KD-induced thrombocytosis and lung inflammation and its mechanism of action.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and methods<\/jats:title>\n                    <jats:p>\n                      C57BL\/6 mice and NLRP3 knockout mice were intraperitoneal injected with\n                      <jats:italic>Lactobacillus casei<\/jats:italic>\n                      cell wall extract (LCWE) to establish models of KD-induced lung inflammation\n                      <jats:bold>.<\/jats:bold>\n                      MEG-01 cells were also stimulated with LCWE, and subsequently intervened with phillyrin and NLRP3 inhibitor MCC950. The therapeutic effects and mechanisms of phillyrin werestudied both\u00a0in vivo and in vitro.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In the LCWE-induced mice lung inflammation model, phillyrin dose-dependently decreased circulating platelet counts and reduced CD61\u207a platelets in lung tissue. Hematological analysis demonstrated that phillyrin administration led to a significant reduction in white blood cell count. Furthermore, histopathological examination revealed attenuated inflammatory infiltration and fewer F4\/80\u207a macrophages in lung sections. Bioinformatic and molecular docking analyses indicated a strong association between phillyrin's effects and the NLRP3\/IL-1\u03b2 axis. Mechanistic studies demonstrated that phillyrin suppressed megakaryocyte-derived platelet production by inhibiting NLRP3 inflammasome-mediated IL-1\u03b2 secretion, which consequently disrupts IL-1\u03b2-driven NF-E2 expression and leads to substantial downregulation of NF-E2. Furthermore, the suppressive effects of phillyrin on megakaryocytic platelet generation and pulmonary inflammation were consistently enhanced in NLRP3-knockout mice, as well as in MEG-01 cells following either NLRP3 inactivation or IL-1 receptor antagonist treatment.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Phillyrin significantly attenuated LCWE-induced lung inflammation and suppressed megakaryocyte-derived platelet production by inhibiting the NLRP3\/IL-1\u03b2 axis, thereby impeding IL-1\u03b2-mediated NF-E2 expression and subsequent thrombopoiesis. These findings identify Phillyrin as a promising therapeutic candidate for Kawasaki disease by targeting the NLRP3\/IL-1\u03b2\/NF-E2 pathway to ameliorate pathological platelet overproduction and pulmonary complications.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Graphical abstract<\/jats:title>\n                    <jats:p>Phillyrin significantly alleviated LCWE-induced pulmonary inflammation by suppressing megakaryocyte-derived platelet production. Mechanistically, phillyrin inhibited the activation of the NLRP3 inflammasome, thereby impeding caspase-1 maturation and IL-1\u03b2 secretion. The blockade of IL-1\u03b2 binding to its receptor consequently downregulated the expression of NF-E2, a pivotal transcription factor regulating platelet production.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s13020-026-01348-6","type":"journal-article","created":{"date-parts":[[2026,3,7]],"date-time":"2026-03-07T01:03:17Z","timestamp":1772845397000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Phillyrin alleviates Kawasaki disease-induced lung inflammation by inhibiting platelet production through the NLRP3\/IL-1\u03b2\/NF-E2 signaling pathway"],"prefix":"10.1186","volume":"21","author":[{"given":"Da-Hao","family":"Mai","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaojie","family":"Huang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Minsi","family":"Liang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiaoyin","family":"Yu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei","family":"Hao","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Long-Wei","family":"Yang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jing-Rui","family":"Feng","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Xiao-Le","family":"Ling","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ke","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Li","family":"Zhu","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yang","family":"Chen","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2026,3,7]]},"reference":[{"issue":"4","key":"1348_CR1","doi-asserted-by":"publisher","first-page":"251","DOI":"10.18176\/jiaci.0300","volume":"29","author":"Y Sakurai","year":"2019","unstructured":"Sakurai Y. 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