{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T05:05:55Z","timestamp":1784264755543,"version":"3.55.0"},"reference-count":57,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T00:00:00Z","timestamp":1784246400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Coronary microvascular dysfunction (CMD) secondary to myocardial ischemia-reperfusion injury (MIRI) is characterized by profound inflammatory activation and endothelial impairment. Guanxinjing compound (GXJC) is a clinical drug widely used for coronary heart disease and angina pectoris closely associated with coronary microvascular function. Its efficacy and mechanisms against MIRI-induced CMD remain elusive.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The chemical profiling of GXJC was performed via UHPLC-Q-Exactive HRMS. Network pharmacology analysis (NPA) screened the core targets and key pathways of GXJC.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , C57BL\/6 mice received 7-day GXJC pretreatment before MIRI modeling, followed by comprehensive evaluation using Evans blue\/TTC staining, Hematoxylin and eosin staining (H&amp;amp;E), apoptosis assessment by TUNEL staining, immunofluorescence, Western blotting, and ELISA. For\n                      <jats:italic>in vitro<\/jats:italic>\n                      studies, a TNF-\u03b1-induced inflammatory injury model in HUVECs was established to dissect the underlying mechanisms.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      UHPLC-Q-Exactive HRMS analysis identified 256 bioactive compounds in GXJC. NPA predicted the TNF signaling pathway as a potential key mechanism through which GXJC may ameliorate MIRI.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , GXJC treatment reduced myocardial infarct size and cardiomyocyte apoptosis while downregulating pro-inflammatory factors. Mechanistically, GXJC suppressed vascular inflammation by inhibiting IL-6, IL-1\u03b2, and CCL2, attenuated endothelial contractile and diastolic dysfunction by modulating the eNOS\/NO\/ET-1 axis, and alleviated endothelial injury and thrombosis by lowering FGL2 and p-selectin levels.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our study demonstrates that GXJC acts as a potential therapeutic agent\u00a0for MIRI-induced myocardial injury and associated microvascular endothelial dysfunction through the dual modulation of inflammatory cascades and\u00a0microvascular endothelial protection. These mechanistic insights support its\u00a0future clinical development for microvascular complications following revascularization.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1846953","type":"journal-article","created":{"date-parts":[[2026,7,17]],"date-time":"2026-07-17T04:24:00Z","timestamp":1784262240000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Guanxinjing ameliorates coronary microvascular dysfunction in myocardial ischemia-reperfusion injury by alleviating inflammation and restoring endothelial function"],"prefix":"10.3389","volume":"17","author":[{"given":"Yaoting","family":"Wang","sequence":"first","affiliation":[{"name":"College of Life Science, Zhejiang Chinese Medical University","place":["Hangzhou, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lan","family":"Li","sequence":"additional","affiliation":[{"name":"School of Medical Technology and 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