{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T06:09:05Z","timestamp":1789711745910,"version":"4.0.1"},"reference-count":68,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T00:00:00Z","timestamp":1789689600000},"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. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Diabetic retinopathy (DR) is a metabolic eye disease closely linked to inflammation and oxidative stress, potentially causing vision decline or blindness. Scutellarin (SCU), a major flavonoid extracted from Erigeron breviscapus, possesses anti-inflammatory and antioxidant properties; however, its protective mechanisms against retinal M\u00fcller cell (RMC) injury in DR remain unclear.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To investigate the protective effects and underlying mechanisms of SCU against high-glucose(HG)-induced edema and inflammation in retinal M\u00fcller cells (RMCs).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Materials and Methods<\/jats:title>\n                    <jats:p>\n                      Primary RMCs were isolated from newborn 3\u20135-day-old Sprague-Dawley (SD) rats and exposed 100\u00a0mmol\/L HG to establish an\n                      <jats:italic>in vitro<\/jats:italic>\n                      injury model. Groups included control, model (HG), low-dose (HG+25\u00a0\u03bcmol\/L SCU), and high-dose (HG+50\u00a0\u03bcmol\/L SCU). Cell viability, migration capacity, Na\n                      <jats:sup>+<\/jats:sup>\n                      -K\n                      <jats:sup>+<\/jats:sup>\n                      -ATPase activity, and apoptosis were assessed using CCK-8 assays, scratch wound healing assays, enzymatic activity assays, and flow cytometry, respectively. The expression and distribution of AQP4, Kir4.1, and molecules associated with the TLR4\/MyD88\/NF-\u03baB\/VEGFA pathway were evaluated via immunofluorescence, Western blot, and qRT-PCR.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      HG exposure significantly suppressed RMC viability, induced apoptosis, disrupted the functional coupling of AQP4\/Kir4.1, and activated the TLR4\/MyD88\/NF-\u03baB\/VEGFA signaling pathway. SCU treatment dose-dependently reversed these pathological changes, restored Na\n                      <jats:sup>+<\/jats:sup>\n                      -K\n                      <jats:sup>+<\/jats:sup>\n                      -ATPase activity and the expression balance of AQP4\/Kir4.1, and inhibited the excessive activation of the inflammatory pathway.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The protective effects of SCU are significantly associated with the restoration of AQP4\/Kir4.1 homeostasis and the suppression of the TLR4\/MyD88\/NF-\u03baB\/VEGFA pathway, suggesting its potential as a multi-target candidate drug for delaying the progression of DR.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1923023","type":"journal-article","created":{"date-parts":[[2026,9,18]],"date-time":"2026-09-18T05:36:55Z","timestamp":1789709815000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Scutellarin attenuates high glucose-induced edema and inflammation in retinal M\u00fcller cells via AQP4\/Kir4.1 restoration and TLR4\/MyD88\/NF-\u03baB inhibition"],"prefix":"10.3389","volume":"17","author":[{"given":"Yunhua","family":"Tang","sequence":"first","affiliation":[{"name":"Eye School of Chengdu University of TCM","place":["Chengdu, Sichuan, China"]},{"name":"Ziyang Hospital of Traditional Chinese Medicine","place":["Ziyang, Sichuan, China"]},{"name":"Key Laboratory of Sichuan Province Ophthalmopathy Prevention and Cure and Visual Function Protection with TCM Laboratory","place":["Chengdu, Sichuan, China"]},{"name":"Retinal Image Technology and Chronic Vascular Disease Prevention and 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