2026-10-13T22:31:30Z https://api.figshare.com/v2/oai

oai:figshare.com:article/33920446 2026-09-18T05:36:28Z category_19 portal_316 item_type_3 month_year_09_2026

Table 1_Scutellarin attenuates high glucose-induced edema and inflammation in retinal Müller cells via AQP4/Kir4.1 restoration and TLR4/MyD88/NF-κB inhibition.docx Yunhua Tang (8376537) Shan Ding (3446876) Wenyan Peng (3625874) Meichu Wu (25070179) Yongqi Mao (22520079) Wenxin Yang (5821358) Xiaoyang Li (1316730) Fuwen Zhang (575612) Pharmacology AQP4/Kir4.1 diabetic macular edema diabetic retinopathy retinal Müller cells Scutellarin TLR4/MyD88/NF-κB/VEGFA Background<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 Müller cell (RMC) injury in DR remain unclear.</p>Objective<p>To investigate the protective effects and underlying mechanisms of SCU against high-glucose(HG)-induced edema and inflammation in retinal Müller cells (RMCs).</p>Materials and Methods<p>Primary RMCs were isolated from newborn 3–5-day-old Sprague-Dawley (SD) rats and exposed 100 mmol/L HG to establish an in vitro injury model. Groups included control, model (HG), low-dose (HG+25 μmol/L SCU), and high-dose (HG+50 μmol/L SCU). Cell viability, migration capacity, Na⁺-K⁺-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-κB/VEGFA pathway were evaluated via immunofluorescence, Western blot, and qRT-PCR.</p>Results<p>HG exposure significantly suppressed RMC viability, induced apoptosis, disrupted the functional coupling of AQP4/Kir4.1, and activated the TLR4/MyD88/NF-κB/VEGFA signaling pathway. SCU treatment dose-dependently reversed these pathological changes, restored Na⁺-K⁺-ATPase activity and the expression balance of AQP4/Kir4.1, and inhibited the excessive activation of the inflammatory pathway.</p>Conclusion<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-κB/VEGFA pathway, suggesting its potential as a multi-target candidate drug for delaying the progression of DR.</p> 2026-09-18T05:36:28Z Dataset Dataset 10.3389/fphar.2026.1923023.s001 https://figshare.com/articles/dataset/Table_1_Scutellarin_attenuates_high_glucose-induced_edema_and_inflammation_in_retinal_M_ller_cells_via_AQP4_Kir4_1_restoration_and_TLR4_MyD88_NF-_B_inhibition_docx/33920446 CC BY 4.0