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

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.