{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T13:06:02Z","timestamp":1793192762782,"version":"4.5.0"},"reference-count":56,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,5,19]],"date-time":"2025-05-19T00:00:00Z","timestamp":1747612800000},"content-version":"vor","delay-in-days":138,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,1,1]],"date-time":"2025-01-01T00:00:00Z","timestamp":1735689600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82160835"],"award-info":[{"award-number":["82160835"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82460866"],"award-info":[{"award-number":["82460866"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Mediators of Inflammation"],"published-print":{"date-parts":[[2025,1]]},"abstract":"<jats:p>\n                    Type I interferon (IFN\u2010I), a pivotal component of the host\u2019s innate antiviral immune system, can induce the formation of neutrophil extracellular traps (NETs) and facilitate inflammatory responses. Baicalin exhibits a range of pharmacological activities, including anti\u2010inflammatory and immunomodulatory effects. It has been reported that neutrophil glycolysis plays a pivotal role in the formation of NETs and the regulation of inflammatory response in immune modulation, regulated by IFN\u2010I. However, it remains unclear whether baicalin regulates IFN\u2010I\u2010induced NETs formation through glycolysis. In this study, we induced the formation of NETs\n                    <jats:italic>in vitro<\/jats:italic>\n                    using IFN\u2010I and observed that baicalin significantly reduced the formation of IFN\u2010I\u2010induced NETs. Furthermore, baicalin inhibited the production of pro\u2010inflammatory cytokines, specifically interleukin\u20101 beta (IL\u20101\n                    <jats:italic>\u03b2<\/jats:italic>\n                    ) and interleukin\u20106 (IL\u20106), as well as the generation of reactive oxygen species (ROS) and chemotactic responses. Our findings further indicated that baicalin could inhibit both lactic acid and ATP levels in IFN\u2010I\u2010induced neutrophils, as well as the expression of glycolytic\u2010related proteins, including HK2, HK3, PKM2, and LDHA. Moreover, following the administration of glycolytic agonists insulin, it was observed that heightened glycolytic activity significantly augmented NETs formation and the release of inflammatory cytokines, potentially regulated by PKC\/Raf\/MEK\/ERK and PI3K\/AKT signaling pathways. In conclusion, our findings indicated that baicalin may exert inhibitory effects on IFN\u2010I\u2010induced NETs formation and inflammatory cytokine production by modulating glycolysis, thereby providing further evidence for the potential clinical application of baicalin in the treatment of IFN\u2010I\u2010related inflammatory diseases.\n                  <\/jats:p>","DOI":"10.1155\/mi\/8822728","type":"journal-article","created":{"date-parts":[[2025,5,19]],"date-time":"2025-05-19T04:20:18Z","timestamp":1747628418000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":19,"title":["Baicalin Modulates Glycolysis\n                    <i>via<\/i>\n                    the PKC\/Raf\/MEK\/ERK and PI3K\/AKT Signaling Pathways to Attenuate IFN\u2010I\u2010Induced Neutrophil 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