Superior antiglycation efficacy of silymarin from <i>Silybum marianum</i> in human αA-crystallin: Implications for diabetic cataract prevention

Hyperglycemia activates the polyol pathway, producing fructose, which promotes glycation and denatures α-crystallin, ultimately leading to diabetic cataracts. This study compared the antiglycation effects of SMR and SBN, using a fructose-induced human αA-crystallin glycation model. Through fluorescence analysis, SDS-PAGE, and Western blotting methods, we found that glycation caused αA-crystallin to form fluorescent advanced glycation end products (AGEs), cross-linking AGEs, and Nε-carboxymethyllysine (CML). Results show that SMR (> 20 μg/mL) and SBN (> 100 μg/mL) effectively inhibited cross-linking AGEs and CML formation. At concentrations above 4 μg/mL, both significantly reduced fluorescent AGEs, with SMR showing 91.0 ± 0.8% inhibition and SBN 81.1 ± 1.7% at 100 μg/mL. SMR also outperformed aminoguanidine hydrochloride in reducing carbonyl content at 500 μg/mL. Therefore, SMR exhibited stronger antiglycation and antioxidation properties than SBN, showing potential as a natural health product to prevent diabetic cataract formation.