{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T05:03:08Z","timestamp":1790053388649,"version":"4.0.1"},"reference-count":52,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T00:00:00Z","timestamp":1790035200000},"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. Cardiovasc. Med."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Atherosclerosis (AS) is a major contributor to deaths from cardiovascular diseases. Yiqihuoxue Formula (YQHXF) reflects the traditional Chinese medicine principle of \u201cQi-invigorating and blood-activating.\u201d This study investigates the anti-atherosclerotic effects and mechanism of YQHXF through the signal transducer and activator of transcription 6 (STAT6)\/ peroxisome proliferator-activated receptor gamma (PPAR\u03b3) signaling pathway and macrophage polarization.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      Ultra-high performance liquid chromatography-high resolution mass spectrometry (UHPLC-HRMS) was used to detect the components of YQHXF-containing serum (YQHXF-CS). Using oxidized low-density lipoprotein (ox-LDL), RAW264.7 macrophages were induced into foam cells\n                      <jats:italic>in vitro<\/jats:italic>\n                      and treated with YQHXF-CS. PPAR\u03b3 knockdown was achieved using siRNA. Cell viability, lipid accumulation, macrophage polarization markers, and STAT6\/PPAR\u03b3 signaling were analyzed.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , ApoE\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice fed a high-fat diet (HFD) received low, medium, or high-dose YQHXF or atorvastatin. Serum lipids, aortic plaque area, histopathology, macrophage polarization, and pathway proteins were assessed.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The results showed that YQHXF-CS contained 2,317 components.\n                      <jats:italic>In vitro<\/jats:italic>\n                      , 5% YQHXF-CS enhanced cell viability, reduced lipid droplets, downregulated M1 markers (nitric oxide synthase 2 (\n                      <jats:italic>Nos2)<\/jats:italic>\n                      ,\n                      <jats:italic>tumor necrosis factor (Tnf)<\/jats:italic>\n                      ,\n                      <jats:italic>interleukin 1 beta (Il1b)<\/jats:italic>\n                      ), upregulated M2 markers (\n                      <jats:italic>interleukin 4 (Il4)<\/jats:italic>\n                      ,\n                      <jats:italic>arginase 1 (Arg1)<\/jats:italic>\n                      ,\n                      <jats:italic>transforming growth factor-<\/jats:italic>\n                      \u03b2\n                      <jats:italic>(Tgfb)<\/jats:italic>\n                      , CD163, CD206), and this was accompanied by enhanced STAT6\/PPAR\u03b3 pathway. Moreover, YQHXF-CS partially counterbalanced siRNA-PPAR\u03b3-induced foam cells formation, and this effect was associated with M2 macrophages polarization.\n                      <jats:italic>In vivo<\/jats:italic>\n                      , YQHXF reduced body weight and serum lipid accumulation, diminished aortic plaque area and pathological damage, increased M2 macrophages (CD206\n                      <jats:sup>+<\/jats:sup>\n                      , IL-4, IL-10), and decreased M1 macrophages (CD86\n                      <jats:sup>+<\/jats:sup>\n                      , TNF-\u03b1, IL-1\u03b2). Mechanistically, YQHXF partially restored aortic p-STAT6 and PPAR\n                      <jats:italic>\u03b3<\/jats:italic>\n                      expression.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>YQHXF ameliorates AS, as evidenced by reduced foam cell formation, alleviated vascular lesions, and promotion of anti-inflammatory M2 macrophage polarization; these effects were associated with enhanced STAT6\/PPAR\u03b3 signaling. This validates the theory of \u201cQi-invigorating and blood-activating\u201d and highlights YQHXF's therapeutic potential.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fcvm.2026.1896890","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T04:21:49Z","timestamp":1790050909000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Yiqihuoxue formula improves atherosclerosis by regulating macrophage polarization associated with enhanced STAT6\/PPAR\u03b3 pathway"],"prefix":"10.3389","volume":"13","author":[{"given":"Quan","family":"Xie","sequence":"first","affiliation":[{"name":"Department of Rehabilitation, Hospital of Chengdu University of Traditional Chinese Medicine","place":["Chengdu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binding","family":"Wang","sequence":"additional","affiliation":[{"name":"Chengdu University of Traditional Chinese 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