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Anti inflammatory agents have been found to be beneficial for the treatment of sepsis. Here, we have evaluated the anti\u2010inflammatory activity of seselin in models of sepsis and investigated the underlying molecular mechanism(s).<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p><jats:italic>In vivo<\/jats:italic> therapeutic effects of seselin was evaluated in two models of sepsis, caecal ligation and puncture or injection of LPS, in C57BL\/6 mice. <jats:italic>In vitro,<\/jats:italic> anti\u2010inflammatory activity of seselin was assessed with macrophages stimulated with LPS and IFN\u2010\u03b3. Anti inflammatory actions were analysed with immunohistochemical methods, ELISA and Western blotting. Flow cytometry was used to assess markers of macrophage phenotype (pro\u2010 or anti\u2010inflammatory). Other methods used included co\u2010immunoprecipitation, cellular thermal shift assay and molecular docking.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p><jats:italic>In vivo,<\/jats:italic> seselin clearly ameliorated sepsis induced by caecal ligation and puncture. In lung tissue from septic mice and in cultured macrophages, seselin down\u2010regulated levels of proinflammatory factors and activity of STAT1 and p65, the master signal pathway molecules for polarization of macrophages into the proinflammatory phenotype. Importantly, adoptive transfer of bone marrow\u2010derived macrophages, pretreated with seselin, lowered systemic proinflammatory factors in mice challenged with LPS. The underlying mechanism was that seselin targeted Jak2 to block interaction with IFN\u03b3 receptors and downstream STAT1.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Implications<\/jats:title><jats:p>Seselin exhibited anti\u2010inflammatory activity through its action on Jak2. These results indicated a possible application of seselin to the treatment of inflammatory disease <jats:italic>via<\/jats:italic> blocking the development of the proinflammatory phenotype of macrophages.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.14521","type":"journal-article","created":{"date-parts":[[2018,10,19]],"date-time":"2018-10-19T11:34:53Z","timestamp":1539948893000},"page":"317-333","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Seselin ameliorates inflammation <i>via<\/i> targeting Jak2 to suppress the proinflammatory phenotype of macrophages"],"prefix":"10.1111","volume":"176","author":[{"given":"Lili","family":"Feng","sequence":"first","affiliation":[{"name":"State Key Laboratory of Pharmaceutical Biotechnology, Department of Rheumatology and Immunology, Nanjing Drum Tower Hospital, School of Life Sciences Nanjing University  Nanjing 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