ArticleFrontiers in pharmacology2026
Scutellarin attenuates high glucose-induced edema and inflammation in retinal Müller cells via AQP4/Kir4.1 restoration and TLR4/MyD88/NF-κB inhibition.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: 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. Objective: To investigate the protective effects and underlying mechanisms of SCU against high-glucose(HG)-induced edema and inflammation in retinal Müller cells (RMCs). Materials and Methods: Primary RMCs were isolated from newborn 3-5-day-old Sprague-Dawley (SD) rats and exposed 100 mmol/L HG to establish an Results: 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 Conclusion: 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.
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